Parkinson's disease (PD) is often accompanied by symptoms of gastric dysmotility, such as gastroparesis. Gastroparesis not only seriously affects the life quality of PD patients, but also causes fluctuations in drug absorption rate, exacerbating the motor symptoms of PD. The previous studies of our laboratory have shown that PD model rats also exhibit gastroparesis, with increased pro-inflammatory cytokines in the gastric muscularis. The markers of related neurons were abnormal. Additionally, the contractile protein markers, as well as their transcriptional regulators, were reduced in smooth muscle cells (SMCs). Continuous gastric feeding of Qizhiweitong particles (QZWT) for seven days improved gastric motility in PD rats with gastroparesis by suppressing inflammation. However, whether QZWT can restore neurons in the gastric muscularis and the differentiated phenotype of SMCs remains to be further investigated. In this study, we detected expressions of neuronal markers in the gastric muscularis and contractile markers of SMCs by immunofluorescence staining, Western blotting, and real-time quantitative PCR, and observed the ultrastructure of SMCs by transmission electron microscopy techniques, aiming to explore the potential mechanisms underlying the improvement effect of QZWT on gastric dysmotility in PD rats and provide new ideas for the treatment of PD gastroparesis. Our results showed that after QZWT administration, there was no change in neuronal markers tyrosine hydroxylase, choline acetyltransferase, and neuronal nitric oxide synthase in the muscular layer of gastric corpus of the PD gastroparesis rats. However, compared to the PD rats, the protein and mRNA expression levels of myosin heavy chain 11 and myosin light chain 20 were significantly up-regulated in the smooth muscle layer of gastric corpus of PD rats with QZWT treatment. Furthermore, the protein and mRNA expression levels of serum response factor (SRF), which regulates the transcription of SMC contractile protein genes, as well as the mRNA level of the transcription related cofactor myocardin (MYOCD), were significantly up-regulated. In addition, the ultrastructure feature of gastric corpus showed that the morphology of SMCs in the PD rats with QZWT treatment was improved, displaying clear dense patches and dense bodies. The vacuoles in the SMCs disappeared. These results suggest that QZWT treatment up-regulates the expression of SRF and MYOCD, which may be associated with its effect of inhibiting inflammation, and further increases the expression of contractile proteins and restores the morphology of the SMCs, promoting gastric smooth muscle contractions in PD gastroparesis rats, thereby leading to improved gastric motility.

Diabetic gastroparesis (DGP) is a chronic and frequently underrecognized complication of diabetes mellitus, characterized by delayed gastric emptying in the absence of mechanical obstruction. It represents a clinically significant manifestation of diabetic autonomic neuropathy and arises from a complex interplay of sustained hyperglycemia, oxidative and nitrosative stress, advanced glycation end-product accumulation, impaired insulin/IGF-1 signaling, lipid dysmetabolism, and inflammatory activation. These mechanisms converge to damage autonomic and enteric neurons, reduce interstitial cells of Cajal density, and disrupt gastric smooth muscle function, ultimately leading to impaired and unpredictable gastric motility. Beyond gastrointestinal symptoms, DGP profoundly affects metabolic control. The altered timing and variability of gastric emptying disturb the physiological coordination between nutrient absorption and insulin pharmacokinetics, generating a temporal mismatch that predisposes patients to early postprandial hypoglycemia followed by late hyperglycemia. This pattern increases glycemic variability, complicates insulin dose adjustment, and contributes to oxidative stress and vascular risk. In this narrative review, we examine the current understanding of DGP pathophysiology and its clinical implications for insulin therapy. We discuss diagnostic strategies, nutritional interventions, and pharmacological treatments, with particular attention to insulin timing modulation. We also analyze the emerging role of diabetes technologies, including continuous glucose monitoring and automated insulin delivery systems, as well as future perspectives such as glucose-responsive insulins and regenerative approaches targeting gastric neuromuscular dysfunction. A mechanism-based, personalized therapeutic strategy may improve metabolic stability and patient outcomes.

Gastroparesis (Gp) and cyclic vomiting syndrome are both characterized by nausea and vomiting, with some patients meeting criteria for both disorders. Gastric electrical stimulation (GES) is a potential treatment for patients with Gp refractory to conservative and first-line treatments and can be used in conjunction with surgical pyloroplasty. While the safety and efficacy of GES and pyloroplasty have been demonstrated, minimal literature discusses the implications of dual implantation of GES with an existing implantable electronic device. This case report describes successful combined GES device implantation and surgical pyloroplasty in a patient with an existing implantable cardioverter-defibrillator.

Irritable bowel syndrome (IBS) is a disorder of gut-brain interaction characterised by recurrent abdominal pain or discomfort that is often related to defaecation or associated with a change in stool frequency or form. IBS is common in Australia and affects women more than men. The exact pathophysiology remains unclear, though it can be multifactorial and relate to gastrointestinal dysmotility, post-infection and microbial changes, and a patient's psychosocial background. A positive clinical diagnosis can be made when the Rome V criteria are met, alarm features are absent and simple screening tests (full blood count, C-reactive protein, coeliac serology) are negative. If alarm features are present, further examination, laboratory testing or imaging may be helpful in assessing for organic pathology. Management involves lifestyle and dietary modifications, and psychological and pharmacological therapies. Pharmacological therapy should be individualised to the patient's IBS subtype and symptoms. Examples of drug classes that are used include antispasmodics, osmotic laxatives, antidiarrhoeal drugs and neuromodulators (tricyclic antidepressants). There is insufficient evidence to support the use of therapies such as probiotics, faecal microbiota transplantation, and mesalamine.

Nutritional support and rehabilitative training are crucial for functional recovery in stroke patients with dysphagia. Malnutrition often aggravates motor, cognitive, and emotional deficits, underscoring the need for tailored nutritional strategies to improve swallowing and motor outcomes. We present a case of severe dysphagia complicated by secondary gastroparesis following a medullary infarction. After assessment by a multidisciplinary team (MDT), a multimodal rehabilitation protocol was implemented, consisting of repetitive transcranial magnetic stimulation (rTMS), transcranial direct current stimulation (tDCS), and neuromuscular electrical stimulation (NMES), combined with conventional swallowing training. Concurrently, a structured stepwise nutritional management plan was executed, progressing from nasojejunal (NJ) feeding to intermittent oro-esophageal (IOE) tube feeding, and finally to independent oral intake. After 3 months of integrated treatment, the patient's Modified Mann Assessment of Swallowing Ability (MMASA) score improved from 81 to 94(out of 100). Videofluoroscopic Swallowing Study (VFSS) demonstrated a reduction in laryngeal elevation latency and safe pharyngeal transit, allowing for the successful removal of the feeding tube. This case suggests that MDT-guided stepwise nutritional management, when combined with multimodal swallowing rehabilitation, may offer a beneficial and feasible therapeutic approach for severe dysphagia post-medullary infarction. This integrated model successfully balances therapeutic safety with functional recovery, providing a practical framework for breaking the vicious cycle of post-stroke dysphagia and malnutrition.

Superior mesenteric artery (SMA) syndrome is a rare cause of proximal intestinal obstruction resulting from compression of the third portion of the duodenum between the aorta and the SMA. It most commonly occurs in slender individuals or those experiencing rapid weight loss, but presentations can be atypical and diagnostically challenging. We report the case of a 28-year-old female with history of postural orthostatic tachycardia syndrome and gastroparesis who presented with recurrent nausea and intractable vomiting following a 110-lb weight loss after prior obesity. Upper gastrointestinal endoscopy and gallbladder ultrasonography were unremarkable. Computed tomography of the abdomen demonstrated findings consistent with SMA syndrome, including severe narrowing of the aortomesenteric angle and reduced aortomesenteric distance. The patient subsequently underwent robotic-assisted duodenojejunostomy with resolution of symptoms. This case highlights an atypical presentation of SMA syndrome following massive weight loss and demonstrates the feasibility of robotic duodenojejunostomy as an effective treatment option.

We present a rare case of postoperative gastroparesis syndrome (PGS) in a 10-year-old girl following thoracoscopic repair of congenital diaphragmatic hernia (CDH). The patient presented to our institution with a 20-day history of intermittent abdominal pain and vomiting. Thoracoabdominal computed tomography revealed a posterolateral congenital diaphragmatic hernia. Emergency thoracoscopic diaphragmatic repair was performed, after which the patient developed gastroparesis syndrome. The child was given continuous nasogastric suction, prokinetic therapy with domperidone, and acupressure massage at the Zusanli (ST36) acupoint. On the 38th day after the operation, the child was able to remove the nasal-gastric tube and resume normal diet. CDH is typically diagnosed and managed during infancy, with postoperative complications predominantly involving pulmonary hypertension and chronic lung disease. The occurrence of PGS following CDH repair is exceedingly rare. This report reviews the relevant literature to enhance clinicians' awareness of this complication and improve patient outcomes.

Alterations in gastrointestinal function (digestion, absorption, motility, secretion, and elimination) play important roles in the pathophysiology of many gastrointestinal disorders. Food also strongly influences gastrointestinal health and disease. Some foods act as antigens that trigger an enteric immune response, while others can serve as substrates with direct or indirect biological effects. Food can also be metabolized by gut microbes into bioactive molecules that alter physiology. This review discusses the current research evidence and the clinical use of "food as medicine" through dietary therapies for the management of various gastrointestinal conditions, including disorders of gut-brain interaction, eosinophilic esophagitis, celiac disease, inflammatory bowel disease, gastroparesis, and short bowel syndrome with intestinal failure.