Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatic branched-chain alpha-keto acid dehydrogenase complex plays an important role in regulating branched-chain amino acid levels. These compounds are essential for protein synthesis but are toxic if present in excess. When dietary protein is deficient, the hepatic enzyme is present in the inactive, phosphorylated state to allow conservation of branched-chain amino acids for protein synthesis. When dietary protein is excessive, the enzyme is in the active, dephosphorylated state to commit the excess branched-chain amino acids to degradation. Inhibition of protein synthesis by cycloheximide, even when the animal is starving for protein, results in activation of the hepatic branched-chain alpha-keto acid dehydrogenase complex to prevent accumulation of branched-chain amino acids. Likewise, the increase in branched-chain amino acids caused by body wasting during starvation and uncontrolled diabetes is blunted by activation of the hepatic branched-chain alpha-keto acid dehydrogenase complex. The activity state of the hepatic branched-chain alpha-keto acid dehydrogenase complex is regulated in the short term by the concentration of branched-chain alpha-keto acids (inhibitors of branched-chain alpha-keto acid dehydrogenase kinase) and in the long term by alteration in the total branched chain alpha-keto acid dehydrogenase kinase activity.
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PMID:Nutritional and hormonal regulation of the activity state of hepatic branched-chain alpha-keto acid dehydrogenase complex. 263 49

Adult male Fisher rats injected with streptozotocin (Stz) to produce diabetes mellitus demonstrated a significant loss of total body weight associated with adipose and muscle tissue wasting. Paradoxically, intestinal mass and length were increased in Stz-treated rats despite catabolism of other tissues. Concomitant with increased intestinal mass, food and water intake increased significantly in Stz-diabetic animals. Renal weight was not reduced despite the fall in total body weight. It is proposed that the adult Stz-diabetic rat responds to a loss of available insulin by polyphagia, polydipsia, and catabolism of adipose and muscle tissue and that a large percentage of available synthetic fuel is devoted to the production of additional intestinal tissue.
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PMID:Paradoxical organ-specific adaptations to streptozotocin diabetes mellitus in adult rats. 296 40

A 16-year-old boy with insulin-dependent diabetes mellitus since age five years was admitted with severe ketoacidosis, and suffered a cardiorespiratory arrest from which he made a full recovery. He subsequently developed the typical clinical picture of diabetic amyotrophy with painful asymmetrical weakness and wasting of proximal lower limb muscles. Cerebrospinal fluid protein was elevated, and electromyography showed typical changes. Diabetic amyotrophy has not previously been reported in this age group.
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PMID:Adolescent diabetic amyotrophy. 320 32

Clinical findings, symptoms and predisposing factors were studied in 43 patients with oesophageal candidiasis, 40 patients with peptic oesophagitis and 40 normal controls. Oesophageal candidiasis was confirmed cytologically. 2.4% of patients who had undergone gastroscopy had oesophageal candidiasis; only three of them had simultaneous candidiasis of the oral cavity. Cardiac failure, oesophageal varices, hiatus hernia and gastric ulcer were common associated disorders. 42% of patients with candidal oesophagitis were symptom-free. Most common symptoms were vomiting, retrosternal and epigastric pain. Peptic oesophagitis was more frequently associated with symptoms. Predisposing factors were present in 88% of cases of oesophageal candidiasis: alcoholism, hepatic cirrhosis, diabetes mellitus, malignant tumours and other wasting diseases. 18 patients had had treatment with cimetidine; they included all 13 patients whose candidiasis was first detected at check endoscopy.
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PMID:[Candidiasis of the esophagus. Prospective study of incidence, type of complaints and predisposing factors]. 373 73

Although lipoprotein lipase (LPL) is believed to be rate limiting in the catabolism of triglyceride-rich lipoproteins, LPL activity has not correlated with plasma triglyceride concentrations in experimental rat diabetes. To gather more information about this enzyme system in diabetes, LPL activities were measured in representative tissues from control and streptozocin-induced diabetic rats fed fat-free chow and in 48-h-starved animals. The DNA content of each tissue was determined so that LPL activity could be expressed in a way that was unaffected by tissue wasting. Diabetic animals lost approximately 20% of their body mass. Adipose tissue and soleus muscle cell masses were reduced, and there was marked fat atrophy at necropsy. Adipose tissue LPL was decreased in both starved and diabetic animals, whereas skeletal muscle activities were variably affected. Lipase content and distribution among the individual organs were calculated with published data for rat carcass composition. In diabetic rats, total LPL (adipose tissue, muscle, and parenchymal organs) was reduced by nearly two-thirds so that skeletal muscle became the predominant source of LPL. Ketonuria was less frequent in diabetic than in starved rats (P less than .018) despite their severe wasting. Serum triglyceride concentrations were higher in ketonuric than nonketonuric diabetic animals, and severe hypertriglyceridemia was seen exclusively in heavily ketonuric animals. These observations together with published information suggest that plasma triglyceride concentrations in the rat model are determined by a complex interplay between very-low-density lipoprotein synthesis, the capacity of the LPL removal system, properties of the lipoprotein substrate, and other unidentified factors.
Diabetes 1987 Apr
PMID:Relationship of organ lipoprotein lipase activity and ketonuria to hypertriglyceridemia in starved and streptozocin-induced diabetic rats. 381 3

Rats were allowed a free selection of a diet from among separate sources of protein, fat and carbohydrate or were fed a composite diet formulated to approximate the nutrient composition of a commonly used nonpurified diet. Immediately after streptozotocin injections, diabetic rats displayed polyuria, polydipsia and glycosuria as well as elevated fasting plasma glucose levels and glucose intolerance indicative of mild diabetes. Diabetic rats allowed a free choice tended to consume more protein and consumed significantly less carbohydrate than nondiabetics. This pattern of nutrient choice was associated with a reduction of diabetic signs including reduced polyuria, polydipsia and glycosuria. Diabetic rats permitted to choose their diets were not hyperphagic and maintained a slow but steady rate of body weight gain, accompanied by a sparing of body fat stores. In contrast, diabetic rats consuming the composite diet experienced no improvement in diabetic status; these rats displayed a deterioration of fasting plasma glucose, severe polydipsia, polyuria and glycosuria as well as hyperphagia and wasting of fat stores. These data demonstrate that when mildly diabetic rats are given the opportunity to select their own diets, they choose a diet that leads to improvement of their diabetic status.
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PMID:Dietary self-selection patterns of rats with mild diabetes. 388 41

Diabetic diarrhea and steatorrhea occur predominantly in young adult males who have juvenile-onset diabetes mellitus complicated by neuropathy. The presentation is often severe, with nocturnal or postprandial watery diarrhea and tenesmus. Massive malabsorption of fat may occur; however, malabsorption of other nutrients and generalized wasting are quite rare. Because the symptoms are relatively refractory to treatment, it is important to rule out other, more easily treatable causes of this presentation. Bacterial overgrowth, exocrine pancreatic insufficiency, and celiac disease are also associated with diabetes mellitus and can mimic this process. Although the mechanism of diabetic diarrhea and steatorrhea remains unclear, neuropathy, gastrointestinal motor abnormalities, bacterial overgrowth, and bile acid abnormalities have been implicated in the pathogenesis.
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PMID:Small intestinal manifestations of diabetes mellitus. 665 61

Some patients with anorexia nervosa and energy-wasting disorders have been found to be able to use their illness to lose weight. This paper presents two patients with diabetes mellitus and one with ulcerative colitis in whom the illness was complicated by anorexia nervosa.
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PMID:Anorexia nervosa associated with energy-wasting disorders. 668 89

Over the last ten years a large body of information has accumulated which indicates that physiologic changes in the plasma insulin concentration are capable of affecting electrolyte transport by the kidney as well as by variety of other tissues. In the present discussion the effect of insulin on the renal handling of sodium, potassium, phosphate, and calcium is reviewed, with an emphasis on sodium transport (Table 1). An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding.
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PMID:Insulin and renal sodium handling: clinical implications. 701 90

Planning effective strategies of nutritional care for individuals with diabetic renal failure requires consideration of nutritional, social and medical factors. Typically, the diet is limited in protein, sodium, fluid potassium, and phosphorus content. Poor diabetes control in renal failure has been associated with fluid overload; elevated serum triglyceride levels; hyperkalemic episodes; and impaired protein synthesis. A diabetic meal plan, modified to meet the required nutrient restrictions, is, therefore, routinely developed for each individual. Serial monitoring of nutritional indexes in each patient enables early detection of nutritional wasting and is useful in evaluating the effectiveness of corrective dietary measures.
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PMID:Nutritional care of patients with renal failure and diabetes. 705 Feb 17


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