Malnutrition is present in chronic alcoholics. However, how moderate alcohol consumption affects the absorption of nutrients like glutamine has not been investigated. Glutamine, an amino acid, is vital to gastrointestinal health. Glutamine is absorbed via sodium-dependent glutamine co-transport (B0AT1; SLC6A19) along the brush border membrane of absorptive villus cells. Rat intestinal epithelial cells (IEC-18) and sixteen-week-old Sprague Dawley rats were administered the equivalent of a 0.04% blood alcohol content of ethanol (8.64 mM; 2 g/kg) to investigate the effect of moderate alcohol on sodium-glutamine co-transport. Sodium-dependent ³H-glutamine uptakes were performed to measure B0AT1 activity. Inorganic phosphate was measured as a function of Na-K-ATPase activity. Protein expression was analyzed by immunohistochemical and Western blot analysis. Ethanol significantly inhibited sodium-dependent glutamine absorption and Na-K-ATPase activity in enterocytes in vitro and ex vivo. Kinetic studies suggested that the mechanism of inhibition was due to decreased maximal rate of uptake (V_max) of the B0AT1 co-transporter, corresponding to decreased B0AT1 protein expression and secondary to an inhibited sodium-gradient at the cellular level in vitro and ex vivo. In all, moderate ethanol significantly inhibited glutamine absorption at the level of decreased B0AT1 expression at the brush border membrane and a reduced sodium gradient, which may contribute to malnutrition present in chronic alcoholics.

Background/Objectives: Gastric ulcer is a prevalent global gastrointestinal disorder influenced by multiple factors, including excessive alcohol consumption, poor dietary habits, psychological stress, smoking, and the chronic use of non-steroidal anti-inflammatory drugs. Among these, alcohol plays a critical role in gastric mucosal injury by enhancing gastric acid secretion, triggering inflammatory responses, inducing oxidative stress, and promoting epithelial cell apoptosis while simultaneously depleting key protective mediators such as nitric oxide and prostaglandin E₂. Growing interest has focused on medicinal plants as promising sources of novel therapeutic agents for the management of peptic ulcer disease. Methods: This review summarizes commonly used medicinal plants documented in both Ayurvedic and modern medical systems that exhibit ulcer-healing potential. Experimental and preclinical studies indicate that various herbal drugs and plant extracts derived from different plant parts exert significant anti-ulcer effects through multiple mechanisms, including antioxidant activity, modulation of inflammatory pathways, enhancement of mucosal defense, and inhibition of gastric acid secretion. Results: The review further highlights the gastroprotective effects of these herbal remedies as demonstrated in established experimental ulcer models. Conclusions: Exploring plant-based therapies for gastric ulcers offers valuable insights into alternative and complementary treatment strategies. Continued research aimed at identifying bioactive compounds, elucidating their molecular mechanisms, and developing improved formulations may contribute to safer, more effective, and patient-friendly therapeutic options for peptic ulcer management.

Dietary lipid absorption is facilitated by bile acids. In the Zucker rat (ZR) model of obesity, bile acid absorption, mediated by the apical sodium bile acid transporter (ASBT), was increased in villus cells from the distal ileum. However, whether ASBT may be de novo expressed more proximally in the small intestine during obesity to facilitate additional bile acid absorption is not known. For this, starting from the end of the ileum to the mid jejunum, caudal-orally, five intestinal segments of equal length (S1–S5) were separated from lean and obese ZRs (LZR and OZR). Intestinal mucosa obtained from these segments were used for total RNA extraction, RT-qPCR and ³H-TCA uptake. The results showed that bile acid absorption along with the mRNA expression of ASBT and FXR progressively decreased caudal-orally in both LZRs and OZRs but was significantly higher in all small intestinal segments in OZRs. The expression of GATA4 was absent in the distal ileum (S1) in both LZRs and OZRs, but steadily increased along the proximal length in both. However, this steady increase was significantly reduced in the comparative obese proximal intestinal segments S2, S3, S4 and S5. The expressions of bile acid-activated G-protein-coupled bile acid receptor TGR5 and S1PR2 were unaltered in segments S1–S4 but were significantly increased in OZR S5. The paradigm changing observation of this study is that ASBT is expressed more proximally in the small intestine in obesity. This likely increases overall bile acid absorption and thereby lipid absorption in the proximal small intestine in obesity.

Gastric ulcers remain a prevalent gastrointestinal disorder aggravated by physical and psychological stress, which disrupts the balance between mucosal defense and aggressive factors. Conventional treatments, though effective, often produce adverse effects and recurrence. This review consolidates the mechanistic insights into phytochemicals, particularly flavonoids, terpenoids, alkaloids, and saponins that exert anti-ulcer effects through antioxidant, anti-inflammatory, and cytoprotective pathways. Emphasis is placed on their roles in modulating prostaglandin synthesis, nitric oxide signaling, cytokine expression, and H⁺/K⁺-ATPase inhibition. Furthermore, recent experimental evidence from stress-induced gastric ulcer models (WIRS, CRS, HRS) is summarized to correlate specific phytochemical classes with protective outcomes. The review underscores phytomedicines as promising, safer alternatives for managing stress-induced gastric ulcers and encourages future standardization and molecular validation studies.

Gastric ulcer disease remains a significant global health concern, with Helicobacter pylori (H. pylori) infection being a primary etiological factor. Conventional therapies are increasingly limited by antibiotic resistance, treatment failure, and adverse effects. In this context, phytomedicine has emerged as a promising complementary and alternative therapeutic approach. This review systematically discusses the key mechanisms by which phytomedicines enhance gastric mucosal defense, including antioxidant activity, anti-inflammatory modulation, inhibition of urease and bacterial adhesion, suppression of virulence factors, and restoration of epithelial barrier integrity. Plant-derived bioactive compounds demonstrate multi-targeted gastroprotective effects through modulation of oxidative stress, cytokine signaling, prostaglandin synthesis, and tight junction preservation. While preclinical and limited clinical evidence support their therapeutic potential, further well-designed clinical trials and standardized phytochemical formulations are required to validate translational applicability.