Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fashion for a healthy lifestyle, muscular and athletic silhouette change our approach to diet. Sports sculpture highlighting the body forces the consumption of larger quantities of proteins than the commonly recommended optimum protein, which is 1 g/kg b.w./24 hours. Raises the question whether or not damages the kidneys? A protein-rich diet has the same haemodynamic effects on the kidneys as well as starvation. In diabetic nephropathy consumed a moderate reduction of protein slows the progression of renal failure, but such actions are not significant restrictions protein. It seems that the protein intake has adverse effects contained in them, salt (up to 3% by weight!). Persons undergoing dialysis should consume at least 1.5 g protein/kg b.w./24 hours. Even more is recommended for sport's people. Both resistance exercise and aerobic are necessary to maintain proper physical fitness and muscle mass, which provides better and longer survival. Everything is banned in competitive sports is recommended in dialysis: EPO, anabolic steroids, growth hormone.
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PMID:[Cult of the body and the kidneys]. 2036 34

Caloric restriction prolongs the lifespan of many species. Therefore, investigators have researched the usefulness of caloric restriction for healthy lifespan extension. Sirt1, an NAD(+)-dependent deacetylase, was identified as a molecule necessary for caloric restriction-related anti-aging strategies. Sirt1 functions as an intracellular energy sensor to detect the concentration of NAD(+), and controls in vivo metabolic changes under caloric restriction and starvation through its deacetylase activity to many targets including histones, nuclear transcriptional factors, and enzymes. During the past decade, investigators have reported the relationship between disturbance of Sirt1 activation and the onset of aging- and obesity-associated diseases such as diabetes, cardiovascular disease and neurodegenerative disorders. Consequently, a calorie restriction-mimetic action of Sirt1 is now expected as a new therapy for these diseases. In addition, recent studies have gradually clarified the role of Sirt1 in the onset of kidney disease. Its activation may also become a new target of treatment in the patients with chronic kidney disease including diabetic nephropathy. In this article, we would like to review the role of Sirt1 in the onset of kidney disease based on previous studies, and discuss its possibility as the target of treatment in diabetic nephropathy.
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PMID:Anti-aging molecule, Sirt1: a novel therapeutic target for diabetic nephropathy. 2336 87

Diabetic nephropathy is the leading cause of end-stage renal disease worldwide. The multipronged drug approach still fails to fully prevent the onset and progression of diabetic nephropathy. Therefore, a new therapeutic target to improve the prognosis of diabetic nephropathy is urgently required. Nutrient-sensing signals and their related intracellular machinery have evolved to combat prolonged periods of starvation in mammals; and these systems are conserved in the kidney. Recent studies have suggested that the activity of three nutrient-sensing signals, mTORC1, AMPK, and Sirt1, is altered in the diabetic kidney. Furthermore, autophagy activity, which is regulated by the above-mentioned nutrient-sensing signals, is also altered in both podocytes and proximal tubular cells under diabetic conditions. Under diabetic conditions, an altered nutritional state owing to nutrient excess may disturb cellular homeostasis regulated by nutrient-responsible systems, leading to exacerbation of organelle dysfunction and diabetic nephropathy. In this review, we discuss new findings showing relationships between nutrient-sensing signals, autophagy, and diabetic nephropathy and suggest the therapeutic potential of nutrient-sensing signals in diabetic nephropathy.
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PMID:Role of nutrient-sensing signals in the pathogenesis of diabetic nephropathy. 2512 52