A narrative review of gastroparesis in obesity: diagnostic challenges, treatment considerations, and metabolic implications

Introduction

Background

Gastroparesis is a chronic motility disorder that presents with delayed gastric emptying in the absence of mechanical obstruction. While gastroparesis is not yet fully understood, etiologies of gastroparesis are categorized into idiopathic, diabetic, and post-surgical (1). These etiologies often lead to cardinal symptoms of early satiety, abdominal pain, nausea, vomiting, postprandial fullness, distension, belching, and bloating (2). Severity of symptoms and patient outcome measures are assessed through the Gastroparesis Cardinal Symptom Index (GCSI). The GCSI can be especially useful in tracking symptom changes and the effectiveness of therapeutic interventions (3). To diagnose gastroparesis, delayed gastric emptying must be objectively demonstrated through gastric emptying scintigraphy (GES), wireless motility capsule (WMC), and breath testing (1,2). The current consensus on management of gastroparesis follows a systematic step-up approach starting with low-fat and fiber dietary modifications, followed by prokinetic and antiemetic pharmacologic agents. Further interventions include enteral nutritional support, gastric per-oral endoscopic myotomy (G-POEM), intrapyloric botulinum toxin (Botox) injection, gastric electric stimulation (GES), and surgical interventions (4).

Rationale

The rising prevalence of obesity globally has brought to light various associated comorbidities and health issues, including gastrointestinal disorders (5,6). Among these, gastroparesis presents a growing concern among patients with obesity, as unique challenges in diagnosis and management occur. While gastroparesis is thought to give rise to nutritional deficiencies and weight loss, patients with obesity can present differently and require unique strategies to manage their disease (7,8). While there is no established direct causal relationship between obesity and gastroparesis, obesity represents a significant comorbidity that complicates diagnosis and management.

Objective

This review integrates the current understanding of the topic with challenges in caring for patients with gastroparesis and obesity. It addresses the interplay between the physiological changes of these two diseases to address clinical knowledge gaps that contribute to suboptimal patient outcomes. We present this article in accordance with the Narrative Review reporting checklist (available at https://ales.amegroups.com/article/view/10.21037/ales-25-5/rc).

Methods

This narrative review was conducted through a literature search of PubMed, Embase, and Cochrane Library databases from January 2000 to January 2024. The search strategy utilized combinations of medical subject headings (MeSH) terms and keywords, including ‘gastroparesis’, ‘gastric emptying’, ‘delayed gastric emptying’, ‘obesity’, ‘severe obesity’, ‘morbid obesity’, ‘diagnosis’, ‘treatment’, ‘management’, ‘bariatric surgery’, and ‘diabetes’. Additional relevant articles were identified through manual review of reference lists from included studies.

Studies were included if they addressed: (I) gastroparesis diagnosis, treatment, or management; (II) patients with obesity, severe obesity when available; or (III) associations between obesity and gastroparesis. We excluded studies focusing solely on children or adolescents, animal studies without human correlations, and case reports with fewer than five patients. No language restrictions were applied.

The search identified 487 potentially relevant articles, which were screened by title and abstract. After removing duplicates and applying inclusion/exclusion criteria, 108 full-text articles were assessed for eligibility, with 85 ultimately included in this review. The literature search and study selection process are outlined in Table 1.

Etiology and epidemiology

The prevalence of gastroparesis in the United States (US) varies depending on the diagnostic criteria. According to a retrospective cross-sectional analysis by Ye et al. [2022], the standardized prevalence of gastroparesis is 267.7 per 100,000 US adults (8). However, “definite” gastroparesis—defined as cases diagnosed within 3 months of GES testing with symptoms for more than 3 months has a prevalence of 21.5 per 100,000 persons. Other cross-sectional population studies report different figures: Syed et al. [2020] found an overall prevalence of 0.16% in a large population-based study, while Stein et al. estimated that gastroparesis affects over four million Americans, including those with suggestive symptoms (9,10).

Etiologies of gastroparesis include idiopathic, diabetic, and post-surgical. Though idiopathic gastroparesis was previously thought to be the most prevalent type, a retrospective cross-sectional analysis found diabetic gastroparesis as the most common cause at 57.4%, with type 2 diabetes mellitus (T2DM) being more prevalent [type 1 diabetes (T1D), 5.7% and T2DM, 51.7%] (11). Post-surgical gastroparesis accounts for 15% of cases and is a recognized complication of upper abdominal surgeries such as vagotomy, fundoplication, and gastric bypass (11,12). Idiopathic gastroparesis accounted for 11.3% of cases and involves a diagnosis without a cause for delayed gastric emptying and associated symptoms (11).

This high prevalence of diabetic gastroparesis is concerning, given the rise of obesity and T2DM globally. Diabetic gastroparesis is believed to result from Vagus nerve diabetic neuropathy, leading to impaired gastric motility and emptying (1). Hyperglycemia itself without T2DM is known to cause antral hypomotility, gastric dysrhythmias, and delayed gastric emptying (1).

The epidemiological relationship between obesity, diabetes, and gastroparesis reveals significant disease clustering. Obesity functions as an independent risk factor for gastroparesis symptom development, with risk amplification observed in T2DM populations. Epidemiological evidence from a nested case-control study demonstrates that 89% of patients with gastroparesis symptoms and T2DM also present with obesity, indicating substantial comorbidity prevalence and suggesting shared etiological pathways between these conditions (7).

A prospective observational cohort study by Parkman et al. found that 29% of patients with idiopathic gastroparesis were also diagnosed with obesity. Over 48 weeks, 53% of patients with idiopathic gastroparesis maintained weight (within 5% of baseline), 30% gained weight, and 17% lost weight (13). Conversely, in a retrospective cohort study, Kim et al. found that 67.6% of patients with diabetic gastroparesis experienced weight gain compared to 24.3% with idiopathic and 8.1% with post-surgical gastroparesis (14). Further research is needed to better understand how obesity, along with gastroparesis, can impact these weight dynamics.

However, these prevalence estimates may not accurately reflect the true epidemiological burden of gastroparesis in patients with obesity. Diagnostic challenges in this patient population, including symptom overlap with other gastrointestinal disorders and technical limitations of current testing methods, likely contribute to underdiagnosis and incomplete prevalence data. These limitations underscore the need to establish more precise prevalence rates and develop obesity-specific diagnostic approaches for this patient population (8,15).

Pathophysiology

The pathophysiology of gastroparesis in patients with obesity involves several mechanisms:

• Neuromuscular dysfunction: in diabetic gastroparesis, dysfunction in the enteric nervous system, interstitial cells of Cajal, and smooth muscle cells delays gastric emptying and reduces motility. These dysfunctions are further exacerbated by the mechanical effects of increased abdominal fat and altered hormonal and metabolic states (2,4).
• Hormonal and metabolic factors: in patients with obesity, metabolic dysregulation, such as hyperglycemia, can exacerbate gastric dysmotility. Interestingly, while gastroparesis traditionally presents with delayed gastric emptying, evidence suggests that gastric emptying may tend to be more rapid in obesity and some racial groups (16,17). This paradoxical acceleration in gastric emptying can further contribute to postprandial glucose excursions, particularly in patients with both obesity and diabetes. However, as diabetes progresses, autonomic neuropathy can develop, potentially leading to the classic delayed emptying seen in diabetic gastroparesis.
• Oxidative stress and inflammation: increased oxidative stress and inflammation contribute to gastroparesis through elevated pro-inflammatory markers and reduced resident macrophages, resulting in damage to the interstitial cells of Cajal and other components of the enteric nervous system, as evidenced by full-thickness bowel biopsies from patients with obesity and gastroparesis (2,4).
• Autonomic dysfunction: autonomic dysfunction, including altered central processing and vagal neuropathy, is particularly relevant in diabetic patients, where autonomic neuropathy is a common complication (5).
• Hormonal and metabolic factors: in patients with obesity, metabolic dysregulation can exacerbate gastric dysmotility through antral hypomotility and gastric dysrhythmias, further delaying gastric emptying (1).

In summary, in patients with obesity, gastroparesis primarily stems from T2DM, with pathophysiology encompassing neuromuscular dysfunction, oxidative stress, inflammation, autonomic dysfunction, and hormonal imbalances—all collectively contributing to delayed gastric emptying and complex symptomatology observed in these patients.

Clinical presentation

The following symptoms are consistently observed across various etiologies of gastroparesis and are the hallmarks of the disease: vomiting, early satiety, postprandial fullness, bloating, epigastric abdominal pain, regurgitation, and acid reflux (2,3,18,19).

Symptom profile and severity

Patients with obesity and gastroparesis have shown a tendency to present with specific symptom constellations, including severe bloating and loss of appetite, which may be exacerbated by the effects of increased abdominal adipose tissue on mechanical movement and gastric motility (2,18). In a cross-sectional comparative study, Boaz et al. examined symptom distribution in patients with T2DM and neuropathy, comparing those with and without obesity (20). Patients with obesity demonstrated markedly higher prevalence of gastrointestinal symptoms across all domains. Early satiety affected 61.5% of patients with obesity vs. 35.2% without obesity, while postprandial fullness occurred in 63.7% vs. 40.8%, respectively. Bloating emerged as particularly prominent, affecting 70.3% of patients with obesity compared to 49.3% without. Abdominal distention showed similar patterns (71.4% vs. 50.7%). Notably, loss of appetite was paradoxically less common in patients with obesity (17.6% vs. 26.8%), suggesting altered symptom profiles in this population.

Comorbid conditions

Obesity itself is associated with several gastrointestinal and hepatic diseases, such as gastroesophageal reflux disease (GERD), metabolic dysfunction-associated steatotic liver disease (MASLD), gallstones, and pancreatitis (21). In the context of gastroparesis and obesity, however, there is a wide array of comorbid conditions that can complicate care and include:

• T2DM: obesity is a recognized major risk factor for the development of T2DM. Patients with obesity and gastroparesis are more likely to have a diabetic etiology, with T2DM being predominantly observed (20,22).
• Hypertension: hypertension and obesity have a deep association. Specifically in the setting of diabetic gastroparesis, 90.2% of patients with obesity, T2DM, and gastroparesis were hypertensive, compared to 63% of patients without obesity (20).
• Chronic pulmonary disease: chronic pulmonary disease is prevalent in 46.4% of patients with obesity, contributing to the overall comorbidity and management burden (8).
• Peripheral vascular and cardiovascular diseases: peripheral vascular disease is present in roughly 30.4% of gastroparesis patients with obesity (8). The role of atherosclerosis and vasculopathy in obesity is significant, especially in the development of coronary artery disease and heart failure (23,24). Although there is no direct evidence in the literature to suggest these conditions are a component of the development of gastroparesis, they do complicate management (8).
• Sleep-disordered breathing: hypoventilation syndrome and obstructive sleep apnea (OSA) affect 8–20% of patients with obesity referred to sleep centers, and 15.1% of bariatric surgery patients (25,26). In patients with obesity, OSA prevalence reaches 80.9%, with 39.7% of patients experiencing both OSA and GERD—a common gastroparesis comorbidity (27). While studies of these conditions in patients with gastroparesis and obesity are limited, sleep disorder research in patients with obesity frequently reveals gastroparesis as a comorbidity, suggesting a high prevalence of these conditions in this population.
• Depression and anxiety: in gastroparesis, higher incidences of depression and anxiety are present (28). These conditions can exacerbate symptoms such as nausea, vomiting, and abdominal pain and further impair the quality of life of patients and impact their care (28,29).

Weight dynamics

Though obesity can be associated with gastroparesis, the diseases are rarely comorbid due to the symptom profile of gastroparesis. Weight gain in these patients is complex and influenced by higher liquid caloric intake, symptoms of constipation, lower caloric expenditure, and lower basal metabolic rates (BMRs) (13).

Oral caloric intake

Paradoxically, increased oral caloric intake can be seen in gastroparesis patients with obesity compared to patients without obesity (18). This happens because patients often rely on high-calorie liquids, such as smoothies, shakes, juice, and supplemental nutrients, as these are easier to tolerate and digest (30). The combination of increased liquid caloric intake and the standard gastroparesis dietary recommendations (calorie-dense, low-fiber, high-fat meals) creates a cycle that can promote weight gain and potentially worsen gastroparesis symptoms (13). Additionally, pre-existing obesity-related eating patterns may independently contribute to gastroparesis symptom severity. These problematic eating behaviors include consuming larger portion sizes, high-fat meals, late evening eating, and increased processed food intake—all of which can delay gastric emptying and either mimic or exacerbate gastroparesis symptoms. The complex relationship between obesity-specific eating behaviors and gastroparesis remains understudied; however, understanding these patterns could significantly improve dietary management strategies for this patient population (4,31).

Constipation and symptom severity

Constipation is a common symptom associated with gastroparesis, with 34% of patients experiencing severe or very severe constipation (32). Severe constipation is a symptom that is more commonly seen in patients with obesity and can be a predictor of weight gain. In an observational study examining body weight in patients with idiopathic gastroparesis, researchers found that weight gain was positively associated with constipation severity at enrollment among 138 patients followed over 48 weeks (13). Although this association is still not yet fully understood, it is thought to involve reduced bowel movements leading to increased retention and nutrient absorption. In addition, in a prospective observational cohort study by Homko et al., patients with idiopathic gastroparesis who reported lower symptom severity were found to have gained weight compared to those with more severe symptoms (33).

Caloric expenditure

Lower energy and caloric expenditure also contribute to weight gain in patients with gastroparesis and obesity. In the same study by Homko et al., resting energy, exercise-related expenditure, symptoms, and caloric intake were assessed. They found that patients with gastroparesis who gained weight expended fewer calories by physical activity compared to those who lost weight or remained weight neutral (33). In addition, individuals with obesity tend to have a reduced BMR per kilogram of body weight than those without obesity and therefore require fewer calories to maintain physiological functions. This positive energy balance leads to weight gain (34,35).

Diagnosis

The diagnosis and testing of patients with obesity and suspected gastroparesis can present certain challenges and require a combination of clinical evaluation and possible alternative diagnostic testing (36,37).

Clinical evaluation

A comprehensive review of medical history and a thorough physical examination are essential to evaluating a patient for gastroparesis. Symptoms such as nausea, vomiting, early satiety, postprandial fullness, bloating, and upper abdominal pain should be assessed (36). In patients with obesity, more severe bloating and less severe loss of appetite are common and should be noted (7).

The GCSI serves as the standard clinical evaluation tool, comprising nine symptoms organized into three subscales: nausea/vomiting (including nausea, retching, and vomiting), postprandial fullness/early satiety (encompassing stomach fullness, inability to finish normal-sized meals, postprandial fullness, and loss of appetite), and bloating (including bloating sensation and visible abdominal distention). Each symptom is rated on a severity scale from 0 (none) to 5 (very severe), with the total score calculated by averaging subscale means (38,39).

GCSI scores guide clinical management, with scores below 1.0 indicating minimal symptoms manageable through lifestyle modifications, scores of 1.1–2.5 suggesting mild gastroparesis requiring first-line pharmacotherapy, scores of 2.6–3.5 representing moderate disease warranting combination therapy and nutritional assessment, and scores exceeding 3.5 indicating severe gastroparesis where invasive interventions may be considered. A reduction of 1 point or 25% from baseline indicates clinically meaningful improvement (40).

While the GCSI alone is useful for assessing symptom severity, it is not a reliable indicator of delayed gastric emptying and should be used in conjunction with other tools, such as GES, to diagnose gastroparesis (36,41).

GES

GES is the gold standard for testing gastroparesis. Solid gastric emptying studies, specifically recognized by the American Gastroenterological Association as the preferred diagnostic approach, involve monitoring a standardized radiolabeled solid egg white meal using a Tc-99m sulfur colloid tracer over four hours. In this test, the patient eats a standardized radiolabeled meal (either solid or liquid), followed by sequential imaging to measure the rate of gastric emptying at specific intervals over 4 hours (36,42). Sequential imaging is performed at specific intervals to measure gastric emptying rates, with gastroparesis diagnosed when there is 10% or more gastric retention at 4 hours post-scintigraphy. While liquid emptying studies can also be performed, solid studies remain the primary diagnostic modality (3,36,43). Liquid emptying studies can be particularly useful in demonstrating delayed liquid gastric emptying in patients who are symptomatic of gastric stasis but have a normal solid emptying study (44). Despite being considered the reference standard, it is important to recognize that GES has significant limitations. There is often poor correlation between the severity of delayed emptying on GES and the patient’s symptom severity. Day-to-day variability in gastric emptying can also occur in the same patient, and standardization of meal composition and testing protocols across centers remains challenging. These limitations underscore the importance of interpreting GES results within the context of the patient’s overall clinical presentation rather than as an isolated diagnostic criterion (45).

Upper endoscopy

Esophagogastroduodenoscopy (EGD) can be a useful adjunct when the diagnosis is unclear or in ruling out malignancy. It allows clinicians to perform biopsies and visually inspect for other causes of gastric outlet obstruction (36).

Laboratory tests

A basic metabolic panel, liver function panel, and a complete blood count are typically ordered in a diagnostic workup of a patient with gastroparesis to identify any electrolyte imbalances or other metabolic abnormalities. Thyroid function tests may also be performed to rule out hypothyroidism, as it may mimic or exacerbate symptoms of gastroparesis (36). In addition, malnutrition is also assessed in gastroparesis patients through albumin and prealbumin levels to evaluate and manage the nutritional status of the patient (46).

Diagnostic challenges

As aforementioned, diagnostic challenges are seen in patients with obesity with gastroparesis, such as difficulties with GES, which may lead to under-recognition or delayed diagnosis of gastroparesis. Increased abdominal adiposity in patients with obesity presents a technical challenge and can affect image quality and interpretation due to the attenuation of gamma rays used in scintigraphy (47). Interpretation of scintigraphy results can additionally be affected due to anatomical differences in patients with obesity. For instance, these patients tend to have a larger baseline cross-sectional area and increased gastric volume compared to patients without obesity, which can affect the guidelines to assess gastric emptying (48). Furthermore, the GCSI scores may be unreliable: for example, these patients may experience more bloating but less loss of appetite (7,47). This can result in less effective management and progression of the disease state, but can be mitigated with more comprehensive and alternative testing (49).

A diagnostic reproducibility study by Desai et al. studied the reliability of gastric emptying scintigraphy by having 60 patients undergo two gastric emptying studies 15 days apart. The characterization of gastric emptying as normal, delayed, or rapid differed between the two studies in 30% of patients (50). Similarly, in a large prospective study by Pasricha et al. following 944 patients in tertiary care centers over 48 weeks, researchers found that 42% of patients initially diagnosed with gastroparesis were then diagnosed with functional dyspepsia after repeating gastric emptying study at 48 weeks, while 37% of patients initially diagnosed with functional dyspepsia were later diagnosed with gastroparesis (51). These conditions often share overlapping symptoms, including postprandial fullness, early satiety, and bloating, and common pathological features such as CD206⁺ macrophages and interstitial cells of Cajal loss (51). Protocol adherence issues further compound diagnostic variability, with many clinicians deviating from the recommended 4-hour study duration, controlled blood glucose levels, and proper restriction of medications (36). Although the underlying reasons for poor compliance with the standardized protocols are unknown, the variability in GES protocols can lead to inaccurate results and adversely affect patient management. A universal approach allows for standardized interpretation of results, interlaboratory comparisons, and reinforces the test’s validity for clinicians. The variability of GES protocols and results, coupled with the interchangeable features of gastroparesis and functional dyspepsia, emphasizes the importance of a comprehensive clinical evaluation rather than considering gastric emptying studies as a definitive diagnostic tool (36,51).

Alternative diagnostic testing

WMC

The WMC offers an alternative to GES for assessing multi-regional gastric emptying and transit in the context of global dysmotility and slow transit constipation. Unlike scintigraphy, which tracks digestible meal emptying, WMC measures gastric emptying by detecting pH changes as the indigestible capsule passes from the acidic stomach environment to the alkaline duodenum during the phase III activity front of the migrating motor complex. Since the capsule cannot be digested and emptied in the same way as meal-related emptying, it lacks the physiological specificity to assess post-prandial motor contractions that are seen in meal-related gastric emptying disorders, resulting in its replacement by more reliable diagnostic methods like GES (36,52). WMC, however, does offer a unique benefit in patients with obesity, where technical diagnostic challenges may arise more due to its ability to identify extra-gastric transit abnormalities (37). This discrepancy between methods emphasizes the importance of correlating objective test findings with clinical symptoms rather than relying on either diagnostic approach alone.

¹³C-spirulina breath test

The ¹³C-spirulina breath test is a non-invasive alternative to GES that measures gastric emptying by analyzing breath samples after ingestion of a ¹³C-labeled meal (3). Despite the importance of understanding gastric emptying patterns, comprehensive kinetic data remain limited for most patients with obesity and T2DM, as these measurements are rarely performed in routine care. While scintigraphy remains the gold standard, ¹³C breath tests offer practical advantages: no radiation exposure, lower cost, and fewer technical limitations in patients with obesity. These features make breath testing particularly valuable for longitudinal monitoring in this patient population, where repeated assessments may be clinically necessary (30).

Gastric alimetry (GA)

GA, also known as electrogastrography, is a non-invasive method that combines high-resolution mapping of gastric electrical activity with detailed symptom analysis. It improves patient phenotyping in chronic gastroduodenal disorders and shows superior correlations with symptoms compared to traditional gastric emptying tests (53). Electrodes are placed on the skin over the abdomen and record the electrical activity of muscles in the stomach. The patient’s symptoms are also tracked over a several-hour span. Gastric slow waves and contractions are then related to the patient’s symptoms that were being tracked (54).

Treatment and management

The treatment and management of gastroparesis in patients with obesity involves a stepwise multidisciplinary approach, ranging from dietary fiber changes to pharmacologic therapy, and surgical interventions in cases of refractory gastroparesis (18,30,36).

Multidisciplinary approach to care

A multidisciplinary approach focused on a care plan tailored specifically to the patient’s case and needs is essential to the management of patients with obesity and gastroparesis. A care team composed of gastroenterologists alongside surgeons, dietitians, and psychologists can be crucial for ensuring positive outcomes (55). This multidisciplinary approach to care can lead to comprehensive management of gastroparesis and obesity and address the dietary, pharmacologic, and surgical needs of the patient.

Lifestyle changes and dietary modifications

Initial gastroparesis management emphasizes dietary modifications, including reduced fiber and fat intake, increased meal frequency with smaller portions, and higher liquid-to-solid caloric ratios (56). The American Diabetes Association (ADA) recommends this conservative approach, particularly for diabetic gastroparesis, which predominates in patients with obesity (57). Management guidelines advocate avoiding fatty and spicy foods, smoking, alcohol, and carbonated beverages (58,59). Cannabis abstinence is also essential, as its use can precipitate cannabinoid hyperemesis syndrome (CHS), characterized by severe nausea and vomiting episodes (60).

Weight loss can also reduce gastroparesis symptoms and improve clinical outcomes (61). The mechanisms underlying this improvement are multifactorial. Weight reduction decreases chronic low-grade inflammation by reducing pro-inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), which are known to impair smooth muscle function and to compromise the enteric nervous system (62,63). In diabetic gastroparesis, weight loss offers additional benefits through improved insulin sensitivity. Since obesity is a major contributor to insulin resistance, weight reduction can enhance glycemic control, which in turn may improve gastric motility and reduce gastroparesis symptom severity (64,65). Although more research is needed to understand the direct implications of weight loss on gastroparesis outcomes, it is evident that weight loss in patients with obesity in general alleviates certain factors that can exacerbate symptoms of gastroparesis and improve outcomes.

Pharmacological treatment

Prokinetic agents, including metoclopramide, erythromycin, and domperidone, demonstrate efficacy but present risks of neurological and cardiovascular complications (57). Novel therapeutic approaches, such as ghrelin agonists (relamorelin) and 5-hydroxytryptamine receptor 4 (5-HT4) receptor agonists (prucalopride), show potential for improving gastric motility, though additional research is required (66). Despite the established link between obesity as a gastroparesis risk factor, current literature lacks comparative analyses of pharmacological interventions in patients with obesity and gastroparesis, indicating an important research gap in optimizing treatment protocols for this population.

Medical management of gastroparesis includes avoiding medications that impair gastric motility, such as opioids, anticholinergics, and glucagon-like peptide-1 (GLP-1) receptor agonists (67). GLP-1 receptor agonists present two significant considerations in gastroparesis management: patients with autonomic neuropathy often experience diminished gastric-emptying effects, and tachyphylaxis develops with continued use. While initial administration significantly delays emptying, this effect generally attenuates after several weeks of treatment. Therefore, concerns about exacerbating gastroparesis primarily apply during treatment initiation, with minimal evidence for significant effects beyond 20 weeks, explaining why many diabetic patients with delayed emptying ultimately tolerate these medications (36). Semaglutide, a GLP-1 receptor agonist that improves insulin secretion, reduces glucagon levels, and delays gastric emptying, has gained widespread use for T2DM treatment and weight management (68,69). Its gastric-emptying effects raise concerns about gastroparesis risk, particularly in patients with obesity. While the prevalence of GLP-1 agonist use in this patient population remains unknown, 24% of diabetic patients with delayed gastric emptying reported GLP-1 agonist use (70). The clinical implications of GLP-1 receptor agonists warrant careful consideration, especially in patients with diabetes and obesity who are at risk for gastroparesis (70,71).

Surgical and endoscopic treatment

Surgical and endoscopic interventions are reserved for patients with refractory gastroparesis who have failed conservative management. Given that patients with obesity and gastroparesis often present with multiple comorbidities and metabolic complications, careful patient selection is critical. Invasive procedures should only be considered for patients with both objective evidence of gastroparesis (abnormal GES and supportive endoscopic findings) and clinically significant symptoms that substantially impact quality of life, nutrition, or glycemic control. It is crucial to distinguish between asymptomatic delayed gastric emptying and true gastroparesis requiring intervention, as gastric emptying studies do not always correlate with symptom severity. Therefore, invasive approaches should be limited to patients with demonstrable clinical impact from their gastroparesis (61,72).

• Intrapyloric Botox injection: intrapyloric Botox injection promotes gastric emptying through pyloric muscle relaxation via acetylcholine inhibition at the neuromuscular junction. Open-label studies have demonstrated variable efficacy: Bromer et al. and Ezzeddine et al. reported 43% and 52% improvements in gastric emptying and symptom scores, respectively (73,74). However, Arts et al. and Friedenberg et al. found no significant improvement compared to control groups (75,76). Symptomatic improvement typically persists for 1–6 months, with duration varying by patient factors (77,78). While some studies indicate potential benefits, the American Gastroenterological Association currently recommends restricting intrapyloric Botox injections to clinical trials (1). Notably, no studies have evaluated this treatment’s efficacy specifically in patients with obesity.
• G-POEM: G-POEM is a minimally invasive pyloromyotomy technique that enhances gastric emptying through partial or complete incision of the pyloric muscle. This procedure is performed by creating a submucosal tunnel in the gastric antrum, exposing the pyloric ring, and then dividing the pyloric muscle fibers while preserving the serosal layer. The American Gastroenterological Association recommends considering this intervention for select patients with refractory gastroparesis (41). A 47-patient study demonstrated significant improvements: 4-hour gastric retention decreased from 37% to 20% (P<0.03), while GCSI scores improved from 4.6 to 3.3 (P<0.001). The procedure showed comparable efficacy across gastroparesis etiologies: idiopathic (57.4%), diabetic (25.6%), and post-surgical (17.0%) (79). While another study reported an 81.1% clinical response rate at 3–6 months post-procedure with improved quality of life, increased body mass index (BMI) correlated with higher G-POEM failure rates (80). This finding suggests that patients with gastroparesis and obesity, while potential candidates for G-POEM, may face elevated risks of treatment failure or symptom recurrence (80). G-POEM specifically targets pyloric dysfunction, which contributes to delayed emptying in only a subset of gastroparesis patients. The procedure is most effective for those with pyloric spasm or hyperactivity rather than primary gastric body neuromuscular dysfunction. Patients with predominant vomiting symptoms tend to be ideal candidates. Importantly, G-POEM addresses just one mechanism of gastroparesis and is not a universal treatment for all patients with delayed gastric emptying (30,41).
• Gastric electrical stimulation (GES): GES is a surgical intervention that should be reserved for medically refractory gastroparesis and involves electrode placement into the gastric muscularis propria via a laparoscopic approach. Two electrodes are inserted along the greater curvature of the stomach, approximately 10cm proximal to the pylorus, with endoscopic guidance to ensure proper location and depth of electrode insertion (81,82). These electrodes are connected to a neurostimulator to deliver electrical pulses to the gastric muscularis propria, reducing gastroparesis symptoms, particularly nausea and vomiting (30,83,84). GES devices cannot be charged and run on an internal battery, which must be surgically removed and replaced. The complications and risks associated with GES implantation include infection, further surgical interventions, possible explantation, and, most commonly, a need for nutritional access. Interestingly, in patients with a higher BMI, GES has been shown to require subcutaneous pocket revisions and experience device migrations (36,85). Research examining GES efficacy in patients with obesity and medically refractory gastroparesis revealed initial symptom improvement in 90% of patients, with 55% maintaining relief at 23 months (83). While the success rate was lower than the 70–80% observed in patients without obesity, it still represents a clinical benefit. Patient selection also appeared to be an important factor, with diabetic gastroparesis patients showing better outcomes compared to idiopathic cases, where all treatments failed. Although GES proved safe, post-GES care required hospital readmission for gastrointestinal issues in 45% of patients. The treatment effectively managed gastroparesis symptoms in patients with obesity but did not affect BMI (83). Current evidence is limited but suggests comparable symptom improvement efficacy between patients with and without obesity (83,84).
• Pyloroplasty and pyloromyotomy: aimed to improve gastric emptying by surgically incising and relaxing the pylorus to widen it. Both pyloroplasty and pyloromyotomy lead to gastroparesis symptom improvement (18,30,83). A study by Eriksson et al. found that BMI had no significant impact on the efficacy of pyloroplasty (86).
• Gastrojejunostomy: the pylorus is bypassed by creating an anastomosis between the stomach and the jejunum to facilitate gastric emptying (18). Gastrojejunostomy can be beneficial in gastroparesis for patients with and without obesity, but the comparison between the two groups has still not been extensively studied. 71% of patients with obesity post Roux-en-Y gastrojejunostomy (RYGJ) have reported significant symptom improvement and reduction in BMI with a mean reduction of 7.7 kg/m² maintained at 20 months follow-up (83). RYGJ showed minimal complications and was beneficial for patients with idiopathic gastroparesis over other etiologies (86% of successfully treated cases), while also reducing dependence on supplemental nutrition postoperatively (83).
• Sleeve gastrectomy: sleeve gastrectomy is a last resort treatment that involves the laparoscopic removal of two-thirds to three-fourths of the stomach and creates a tubular gastric structure that is based on the lesser curvature (87). Sleeve gastrectomy not only reduces stomach capacity but also induces hormonal changes through the removal of the gastric fundus, the primary site of ghrelin production (87,88). As a treatment for gastroparesis, studies have shown sleeve gastrectomy to be effective. Alicuben et al. showed that 90% of patients with refractory gastroparesis were able to tolerate a regular diet as well as improvements in GCSI, which decreased from 33.6 preoperatively to 14.9 postoperatively (P=0.01) post sleeve gastrectomy (89). Barium Emptying Radiography Index (BERI) (P<0.01) and quality of life measures were used in a study by Lee et al. to study the effects of sleeve gastrectomy on gastric emptying. Gastrointestinal Quality of Life Index (GIQLI) scores increased from 78 preoperatively to 114 postoperatively (P<0.0001) (90). Additionally, a systematic review by Masclee et al. found that sleeve gastrectomy improved symptoms of gastroparesis and gastric emptying in 45% to 67% of patients with refractory gastroparesis (72). Although sleeve gastrectomy is shown to be effective in managing refractory gastroparesis, it is not a standard treatment and requires further research through larger, long-term studies to fully establish the efficacy of treating gastroparesis in patients with obesity.
• High-efficacy gastroparesis procedure for patients with obesity: Roux-en-Y gastric bypass (RYGB) has been demonstrated to significantly improve gastric emptying, weight loss, and symptoms of gastroparesis in patients with obesity. Papasavas et al. showed that RYGB led to marked symptom improvement and facilitated significant weight loss in patients with obesity, with a mean BMI reduction of 9.1 units or 71.6 lbs, with participants no longer requiring prokinetic medications post-operatively (61). Similarly, in a comparative study between gastrectomy with Roux-en-Y reconstruction and Roux-en-Y with stomach left in situ, RYGB with stomach left in situ (RY-SIS) demonstrated strong efficacy in managing gastroparesis, with 92.3% of patients reporting initial symptom relief from nausea and vomiting (91). At 6 months post-operatively, patients showed improvement in nausea, vomiting, bloating, and reflux symptoms, with most improvements maintained at 12 months, and significant quality of life improvements with an average GCSI score of 2.4 maintained at a median of 38.8 months follow-up (91).

It is essential to note that traditional concepts of gastric emptying are fundamentally altered after this procedure. This anatomical rearrangement results in rapid emptying of the small gastric pouch and can lead to dumping syndrome, characterized by post-prandial abdominal pain, nausea, and vasomotor symptoms (61,72,87,92,93). Although the overall complication rate was low at 7.7%, 23.1% of patients required interventions following RYGB, such as feeding tube placement (91). Interestingly, this procedure showed better outcomes for patients with diabetic gastroparesis compared to those with idiopathic etiology. RYGB increases post-prandial GLP-1 levels and fasting peptide YY (PYY), and while GLP-1 is known to delay gastric emptying, the improvement in gastroparesis symptoms post-RYGB is more likely due to bypassing portions of the stomach (94). RYGB is also effective in improving obesity-related comorbidities through weight loss, which is particularly important in patients with obesity and gastroparesis (87,95,96). While procedures such as sleeve gastrectomy have shown efficacy in patients with gastroparesis, current medical literature suggests that RYGB may be particularly beneficial for managing gastroparesis symptoms in patients with obesity, though comparative long-term data remain limited.

• Subtotal or total gastrectomy: the partial or full removal of the stomach can be considered as a last resort option in severe, refractory cases of gastroparesis. This procedure carries a significant risk of perioperative morbidity and complications such as malnutrition and dumping syndrome and generally is advised only after all other treatments have failed (9,43,97). Subtotal or total gastrectomy with Roux-en-Y reconstruction is shown to be highly effective at treating medically refractory gastroparesis, with roughly 70% of patients reporting sustained symptom relief at follow-up (83). This procedure carries a significant perioperative complication rate of 44.4% (91). When compared to RY-SIS, gastrectomy shows equivalent symptomatic improvement but requires fewer subsequent surgical interventions (3.7% vs. 23.1%), suggesting it may be a more definitive solution despite its higher initial morbidity (83,91). Gastrectomy has shown similar efficacy in improving gastroparesis symptoms in patients with obesity compared to those without, but the data is still limited, and further investigation is needed to compare efficacy in various patient populations.

Impact of weight on surgical outcomes

Weight can affect the outcomes and complications of gastroparesis procedures. Patients with obesity tend to have worse surgical outcomes due to multiple comorbidities, increased operative times, blood loss, and higher rates of complications such as post-operative infections, anastomosis leaks, venous thromboembolism, and cardiovascular complications (98-100). In the context of gastroparesis, weight can play a factor in surgical decision-making. Patients are more likely to undergo sleeve gastrectomy or gastric bypass when their BMI is over 35 kg/m² (101). The complications that are most seen in patients with obesity undergoing bariatric surgery for gastroparesis are still unknown and need to be further studied to mitigate these complications for future patients.

Enteral nutrition

Despite intervention, patients with gastroparesis and obesity may continue to experience nutritional compromise, typically manifesting as micronutrient deficiencies rather than global energy deficits (30,36,102,103). Common deficiencies include vitamin B12, vitamin D, iron, calcium, and zinc, which can impact overall health and complicate recovery despite adequate caloric intake. Diagnosis requires a comprehensive laboratory assessment, including complete blood count, iron studies, 25-OH vitamin D, vitamin B12, folate, zinc, magnesium, and pre-albumin levels. Management should include targeted supplementation of identified deficiencies, potentially using liquid or dissolvable formulations to enhance absorption. For severe cases with significant nutritional impact, a nutrition support consultation is warranted to develop individualized supplementation strategies that address specific deficiencies while minimizing gastroparesis symptoms (4,102).

Supplemental nutrition may be considered for patients suffering from nutritional compromise (12,36). Enteral access for gastroparesis can be achieved through several distinct approaches, such as percutaneous endoscopic gastrostomy with jejunal extension (PEG-J), direct percutaneous endoscopic jejunostomy (DPEJ), nasojejunal (NJ)/orojejunal (OJ) tube placement, and surgical jejunostomy. PEG-J tubes are placed using endoscopic guidance and involve inserting a jejunal feeding tube through an existing gastrostomy into the small bowel that bypasses the stomach, allowing for gastric decompression, though they carry risks of tube dislodgement and migration (104). DPEJ provides direct post-pyloric access through endoscopically guided placement of a jejunostomy tube without the need for a prior gastrostomy and is useful in patients with altered anatomy. NJ/OJ tubes are primarily utilized for short-term nutritional delivery (104). Surgical jejunostomy is a more invasive method that provides the most secure and reliable long-term jejunal access. This method can be performed either laparoscopically (lap-J) or through an open procedure (open-J) and is usually reserved for patients who require long-term enteral nutrition and for those where other methods are not appropriate (104,105). Clinical decision making between these methods requires analysis of various factors, including anticipated length of use, patient anatomy, local expertise of staff, and if concurrent gastric decompression is needed (105).

Complications, prognosis, and long-term challenges

The complications of gastroparesis in patients with obesity include continued nutritional deficiencies, poor glycemic control, persistent gastrointestinal symptoms, psychological distress, quality of life changes, and increased healthcare utilization. These complications require a comprehensive and multidisciplinary approach to patient management.

Glycemic control

In diabetic patients, glycemic control is significantly complicated by gastroparesis due to unpredictable gastric emptying. This unpredictability creates timing mismatches between insulin action and carbohydrate absorption—a particular challenge for patients requiring mealtime insulin. Pre-meal insulin may act before delayed food absorption, causing hypoglycemia, while delayed nutrient emptying can lead to hyperglycemia hours after eating. These fluctuations often necessitate adaptive insulin strategies such as post-meal injections or continuous glucose monitoring and represent one of the most prevalent clinical problems in diabetic gastroparesis management (106,107).

Psychological impact

Chronic symptoms and the burden of managing complex conditions like gastroparesis can lead to significant psychological distress, including anxiety and depression. This is compounded in patients with obesity who may already be dealing with body image issues and other obesity-related psychological stressors (108). We recommend that patients with obesity and gastroparesis be closely monitored by a team of gastrointestinal psychologists.

Impact on quality of life

Persistent gastroparesis symptoms such as nausea and vomiting can still significantly impact the quality of life in patients with obesity, affecting eating behaviors and enjoyment of food, social interactions and relationships, and work productivity (9).

Strengths and limitations

Strengths

This review uniquely addresses the understudied intersection of gastroparesis and obesity, utilizing a multidisciplinary approach across gastroenterology, bariatric surgery, endocrinology, and nutrition specialties. It provides practical clinical guidance specifically tailored for patients with obesity while identifying critical knowledge gaps to direct future research efforts. In addition, our review discusses the full spectrum of diagnostic and management challenges as well as alternative diagnostic modalities that can be utilized with this complex patient population.

Limitations

Published data specifically examining this patient population remains limited, with most studies treating obesity as a secondary consideration rather than a primary focus.

With there being a lack of literature, the evidence quality varies throughout the review. Most available evidence comes from retrospective analyses and case series with inherent methodological weaknesses. For example, Sun et al.’s surgical outcomes study examined only 38 patients over a mean follow-up of 23 months, limiting conclusions about long-term efficacy (83). Non-randomized comparisons between treatments carry selection bias that must be considered when interpreting results.

Open-label investigations lacking control groups, including several Botox studies, cannot distinguish true treatment effects from placebo responses. Large database analyses provide valuable epidemiological insights but may miss important clinical distinctions.

The challenge of separating obesity-specific findings from general gastroparesis outcomes further limits definitive conclusions, particularly when obesity subgroups lack the sample size for meaningful analysis.

Conclusions

Gastroparesis in the context of obesity presents unique challenges to care that require a comprehensive, patient-centered approach. These physiological changes in obesity significantly impact both disease presentation and management strategies, with symptoms often differing from traditional gastroparesis presentations. Specifically, the high prevalence of T2DM in this population adds complexity to both diagnosis and management.

The diagnostic process requires careful consideration, as traditional testing methods face technical limitations in patients with obesity and symptom overlap with other gastrointestinal disorders. While alternative diagnostic tools show promise, a standardized approach specific to obesity remains necessary. Treatment strategies must also be individualized, progressing from conservative management to surgical interventions, when necessary, with patient-centered factors guiding the therapeutic approach.

Several critical research priorities have emerged: developing standardized, specific diagnostic protocols, investigating the impact of newer therapeutic agents like GLP-1 agonists, and establishing comprehensive care models that address both conditions effectively. Despite gastroparesis being traditionally associated with weight loss, the growing overlap with obesity necessitates better epidemiological understanding. As the prevalence of obesity continues to rise globally, addressing these identified gaps becomes increasingly crucial for improving outcomes in this growing patient population.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://ales.amegroups.com/article/view/10.21037/ales-25-5/rc

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Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://ales.amegroups.com/article/view/10.21037/ales-25-5/coif). J.T.D. serves as an unpaid editorial board member of Annals of Laparoscopic and Endoscopic Surgery from November 2024 to December 2026. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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