Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Weight loss treatments include diets, drugs, physical training, and surgery, namely bariatric or obesity surgery. The current standard for bariatric surgery is gastric bypass. There are common beliefs that gastric bypass induces body weight loss because of a reduced food intake and that high-fat diet induces overweight and obesity because of overnutrition. The principal aim of the studies on rats summarized herein was to better understand the physiological mechanisms by which gastric bypass achieves body weight loss and by which high-fat diet induces obesity. The results indicated that gastric bypass efficiently reduced body weight, particularly the fat compartment, which was unlikely to be caused by early satiety, reduced food intake or malabsorption, and that large meal size, but not overnutrition, was mainly responsible for high-fat diet-induced obesity. It was unclear whether gastric ghrelin, obestatin and/or amine in the A-like cells were involved in this context.
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PMID:Feeding behavior and body weight development: lessons from rats subjected to gastric bypass surgery or high-fat diet. 2038 43

The collateral effects of obesity/metabolic syndrome include inflammation and renal function decline. As renal disease in obesity can occur independently of hypertension and diabetes, other yet undefined causal pathological pathways must be present. Our study elucidate novel pathological pathways of metabolic renal injury through LDL-induced lipotoxicity and metainflammation. Our in vitro and in vivo analysis revealed a direct lipotoxic effect of metabolic overloading on tubular renal cells through a multifaceted mechanism that includes intralysosomal lipid amassing, lysosomal dysfunction, oxidative stress, and tubular dysfunction. The combination of these endogenous metabolic injuries culminated in the activation of the innate immune NLRP3 inflammasome complex. By inhibiting the sirtuin-1/LKB1/AMPK pathway, NLRP3 inflammasome dampened lipid breakdown, thereby worsening the LDL-induced intratubular phospholipid accumulation. Consequently, the presence of NLRP3 exacerbated tubular oxidative stress, mitochondrial damage and malabsorption during overnutrition. Altogether, our data demonstrate a causal link between LDL and tubular damage and the creation of a vicious cycle of excessive nutrients-NLRP3 activation-catabolism inhibition during metabolic kidney injury. Hence, this study strongly highlights the importance of renal epithelium in lipid handling and recognizes the role of NLRP3 as a central hub in metainflammation and immunometabolism in parenchymal non-immune cells.
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PMID:Metabolic injury-induced NLRP3 inflammasome activation dampens phospholipid degradation. 2858 89