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

The different dietetic measures for weight reduction are described. According to the existing overweight the therapeutic measures are classified in four steps. In the first step, with low overweight, the energy-containing drinks (soft drinks and alcoholic beverages) are avoided. If the overweight is greater an additional reduction of the energy content of meal is required. A real reduction-diet (less than 1.000 Kcal/day or 4.200 KJ/day) demands extensive knowledge of food composition and greater efforts in meal composition. The availability of formula diets is considered as a relief. During starvation (or total fasting) as the step 4 of weight reduction diet, an extreme metabolic alteration takes place, which is characterized by ketosis. The same metabolic alteration is found by a fat-protein-diet (a so-called ketogenic diet), where hypercholesterolemia and hyperuricemia are common side effects. The carbohydrate-protein weight reduction diet is poor in health risks. Furthermore the normal metabolic pattern is maintained during this kind of diet if enough carbohydrates are provided per day (i.e. 80-100 g/day).
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PMID:[Possibilities for weight reduction by means of diet]. 48 76

Acute urate nephropathy during starvation for weight reduction has been observed in 2 patients. Under these conditions ketoacidosis causes impaired renal uric acid excretion and hyperuricemia. Uricosuric agents or sudden intake of normal calorie diet induces massive uricosuria and kidney damage. Uricosuric agents should be avoided and steps taken to promote abundant diuresis, while allopurinol should be prescribed.
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PMID:[Acute kidney failure as a complication of fasting therapy]. 89 46

The provision of small amounts of glucose during fasting is known to spare body protein and to attenuate markedly the metabolic response to starvation. These actions, which are not shared by fat, are generally thought to depend on the ability of exogenous glucose to stimulate insulin secretion. To determine whether fructose, a very weak insulin secretagogue, will also conserve nitrogen and alter the response to fasting, we infused small amounts of fructose, 100 g/d (375 kcal), into 7 obese subjects during a 10-day fast: 4 received fructose days 7 to 10, and 3 received fructose days 1 to 7. Fructose virtually abolished (all P less than 0.05-0.01) the fasting induced: (a) fall in glucose and insulin and rise in glucagon, (b) fall in triiodothyronine, (c) ketosis and acidosis, (d) increased ammonia excretion, (e) hyperuricemia (and hypouricosuria), and (f) fall in plasma alanine and rise in branched chain amino acids. Fructose also significantly reduced urinary sodium loss. Moreover, fructose exerted a prominent protein-sparing action, even though plasma insulin concentrations never exceeded postabsorptive levels. Excretion of total nitrogen was reduced by 40% to 50% during periods of fructose infusion, reflecting significant suppression of both urea and ammonia generation (all P less than 0.05-0.01). Most plasma glucogenic amino acids rose significantly during fructose administration. We conclude that low-dose fructose infusion essentially abolishes the entire hormone-substrate response to fasting, and spares body protein without raising insulin above postabsorptive levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitrogen conservation in starvation revisited: protein sparing with intravenous fructose. 351 Mar 63

The development of very-low-calorie diets (VLCD) over the lats 50 years is described, from the early work of the Pittsburgh group in 1930, using conventional food, to the present day liquid-formula diets containing all essential nutrients. Recent work has been concerned with the protein requirements of obese patients consuming 200-400 kcal (0.8-1.6MJ) VLCD. Independent studies indicate that the protein requirement is about 40-55 g/day without carbohydrate, and about 25-30 g/day when carbohydrate (30-45 g/day) is included. Although some workers use VLCD consisting only of protein, the author prefers those also containing carbohydrate because they prevent excessive ketosis, hyperuricemia, diuresis, electrolyte loss, re-feeding oedema, and may improve muscular endurance. Numerous clinical trials have shown VLCD to be highly effective in about 80 per cent of outpatients and give an average weight loss of 2 kg/week which is comparable to that seen in complete starvation. Clinical studies of up to 16 weeks and longer in numerous medical schools in Europe have demonstrated their safety in patients under medical supervision. Whilst the achievement of a normal body weight in most obese patients is now a reality, the main problem for the future is to achieve permanent weight loss.
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PMID:The historical development, efficacy and safety of very-low-calorie diets. 702 53

GLUT9 is a novel, facilitative glucose transporter isoform that exists as two alternative splice variants encoding two proteins that differ in their NH(2)-terminal sequence (GLUT9a and GLUT9b). Both forms of GLUT9 protein and mRNA are expressed in the epithelia of various tissues; however, the two splice variants are expressed differentially within polarized cells, with GLUT9a localized predominantly on the basolateral surfaces and GLUT9b expressed on apical surfaces. Protein expression of GLUT9 drops under conditions of starvation but increases with addition of glucose and under hyperglycemic conditions. The substrate specificity of GLUT9 is unique since, in addition to transporting hexose sugars, it also is a high-capacity uric acid transporter. Several recent large-scale human genetic studies show a correlation between SNPs mapped to GLUT9 and the serum uric acid levels in several different cohorts. The relationship between GLUT9 and uric acid is highly clinically significant. Elevated uric acid levels have been associated with metabolic syndrome, obesity, diabetes, hypertension, and chronic renal failure. Although some believe uric acid is elevated as a result of these diseases, there is now evidence that uric acid may play a role in the pathogenesis of these diseases. It is also known that GLUT9 is expressed in articular cartilage and is a uric acid transporter, and thus it is possible that GLUT9 plays a role in gout, a disease of uric acid deposition in the joints. In addition, some studies have suggested that intake of fructose plays an important role in causing elevated serum uric acid levels, especially in diabetes and obesity. It is possible that GLUT9, which seems to be both a fructose and a uric acid transporter, plays an important role in these conditions associated with hyperuricemia.
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PMID:Facilitative glucose transporter 9, a unique hexose and urate transporter. 1979 40

We reviewed lifestyle factors that influence serum uric acid levels and risk of gout flare, and how to improve their deleterious effects. Since obesity increases uric acid and weight gain increases gout risk, weight reduction by daily exercise and limiting intake of excess calories is recommended. However, strenuous exercise, which causes adenine nucleotide degradation; starvation, which decreases uric acid excretion; and dehydration may raise the level of uric acid in serum and trigger gout. Increased intake of purine-rich foods, such as meat and seafood, raise the level of uric acid in serum and is associated with increased risk of gout, whereas dairy products, especially low-fat types, are associated with a lower risk of gout. Also, heavy alcohol drinking raises the uric acid level and increases the risk of gout through adenine nucleotide degradation and lactate production. Sweet fruits and soft drinks containing fructose should be moderated, since fructose may raise uric acid and increase gout risk through uric acid production and/or decreased excretion. On the other hand, the Mediterranean diet is recommended for gout patients, since it may also help prevent hyperuricemia. Furthermore, coffee and vitamin C supplementation could be considered as preventive measures, as those can lower serum uric acid levels as well as the risk of gout.
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PMID:Nonpharmacological Management of Gout and Hyperuricemia: Hints for Better Lifestyle. 3020 51