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The obesity pandemic continues to increase in prevalence in children and adolescents, with its increase outpacing the rate of adult obesity; the human developmental index, body mass index, and family income all display associations to childhood obesity. There are numerous adverse complications of childhood obesity, including cardiovascular, endocrine, and gastrointestinal manifestations. Obesity is thought to be an interaction of several different factors, such as leptin, proopiomelanocortin, glucose uptake in adipocytes, melanocortin receptor 4, protein convertase 1/3, brain-derived neurotrophic factor, fat-mass and obesity-associated gene, melanocortin receptor 4, tumor necrosis factor, interleukin-6, and long noncoding RNA. Epigenetic regulation, the unique gut microbiome role in contributing to obesity, environmental factors, and the social context of a child can precipitation of childhood obesity. In this review, we hope to explore the different medications for obesity, orlistat, glucagon-like peptide-1 agonists, liraglutide, semaglutide, exenatide, setmelanotide, metreleptin, naltrexone, lorcaserin, phentermine, metformin, fluoxetine, lisdexamfetamine, and zonisamide, while also reviewing surgeries such as the Roux-en-Y gastric bypass, laparoscopic or vertical sleeve gastrectomy, and adjustable gastric banding. Show less

Semaglutide (SEM) is a glucagon-like peptide-1 (GLP-1) receptor agonist formulated for oral delivery with the absorption enhancer salcaprozate sodium (SNAC). Although oral SEM achieves 0.4-1% bioavailability through gastric epithelial uptake, gastrointestinal (GI) adverse events remain a major cause of therapy discontinuation. This study examined the effects of SEM (0.74 mg/kg/day), SNAC (22 mg/kg/day), and combined SEM-SNAC (1:33 w/w) treatments on microbiota and metabolic function, in healthy Sprague Dawley rats over 21 days. Whilst microbial α-diversity remained stable, SNAC significantly altered β-diversity (PERMANOVA, p < 0.05) and depleted primary fermenters in Muribaculaceae (-62%) and Bacteroidaceae (-77%) compared to the control group. These compositional changes correlated with reduced predicted saccharolytic enzyme abundance and fecal butyrate concentrations (-77% SNAC, -75% SEM-SNAC). Plasma cytokine analysis showed elevated tumor necrosis factor-α (TNF-α, 70%) and suppressed brain-derived neurotrophic factor (BDNF, 85%), consistent with changes in circulating inflammatory and neurotrophic markers from SNAC monotherapy. SNAC-treated animals also exhibited increased liver weight and reduced caecum mass, occurring alongside microbiota compositional changes and altered fermentation-associated markers. Spearman correlations linked Muribaculaceae and Bacteroidaceae loss with decreased saccharolytic enzyme abundance, lower SCFA levels, and increased TNF-α. While these findings are associative and require mechanistic validation, they indicate that chronic SNAC exposure is linked to concurrent microbial, metabolic, and inflammatory marker changes in healthy rats, highlighting the potential need for alternative, microbiota-safe strategies for oral peptide delivery. Show less

Crocetin (CRT), one of the active ingredients in saffron, exerts health-promoting effects on body systems such as neuroprotective, cardioprotective and hepatoprotective properties. In the present study, the effects of CRT and lansoprazole (LAP), as a reference drug, were investigated on indomethacin (IND)-induced gastric ulcer and related anxiety. Thirty rats were divided into five groups of six. Groups 1 and 2 received vehicle and groups 3, 4 and 5 received CRT (5 and 20 mg/kg) and LAP (30 mg/kg) for seven consecutive days. All groups were deprived of food on day 6. On day 7, group 1 was treated with vehicle and groups 2, 3, 4 and 5 received 50 mg/kg IND. Anxiety and locomotor activity were recorded, and then the animals were euthanized and stomach and hippocampus samples were taken. The effects of the aforementioned treatments were studied in 24 intact rats in four equal groups. CRT (20 mg/kg) and LAP restored IND-induced alterations in the gastric content volume and pH and ulcer index and protection and cyclooxygenases 1 and 2 and prostaglandin E2 and gastric mucosal and hippocampal superoxide dismutase, malondialdehyde, tumor necrosis factor-alpha, interleukin-1β and caspase-3 and hippocampal brain derived neurotrophic factor. Histopathological alterations in the gastric mucosa and hippocampus were improved, and anxiety was suppressed. Intact rats were not influenced. CRT and LAP caused protective effects against IND-induced gastric ulcer and by antioxidative, anti-inflammatory, anti-apoptotic and PGE Show less