Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:034761 (insulin)
 211,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of alcoholic ketoacidosis in a 23-year-old chronic alcoholic, gravada V, para IV, is reported. Symptoms were constant, severe, nonradiating pain with crampy exacerbations, anorexia, nausea and vomiting. The patient had a tender and irritable full-term uterus. She was treated inhospital with vigorous fluid therapy and 5% dextrose in normal saline, sodium bicarbonate, glucose and insulin and showed improvement overnight. Alcoholic ketoacidosis has not been reported in pregnant women. Metabolic derangements combine to produce ketoacidosis more readily in the pregnant alcoholic. Differentiation of alcoholic ketoacidosis and diabetic ketoacidosis is important since treatment varies. For alcoholic ketoacidosis, treatment is vigorous rehydration with dextrose-saline while diabetic ketoacidosis usually requires multiple therapeutic modalities.
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PMID:Alcoholic ketoacidosis in a pregnant woman. 11 97

Hepatic-portal infusions of isotonic glucose did not influence food intake in free-feeding rabbits. In contrast, several other macronutrients and some of their metabolites, infused via the same route, cause anorexia followed by prolonged hypophagia. Its duration was generally decreased when the same infusions were performed during the nocturnal period. Vagotomy did not significantly alter the food intake responses to hepatic-portal infusions of either glucose or the other experimental substances. The results of related experiments have demonstrated that prolonged anorexia was not a consequence of the fast infusion rate or the generalized behavioral mallaise. However, when the infusions of most anorexigenic substances were followed by intraperitoneal administration of insulin, the duration of anorexia was shortened and food consumption was elevated. The results provided indirect evidence for the vagally mediated regulatory contribution of the previously studied neural and humoral intestinal mechanisms which are bypassed by infusing nutrient loads directly into the hepatic-portal circulation.
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PMID:Hepatic-portal nutrient infustion: effect on feeding in intact and vagotomized rabbits. 55 91

Rats that were made diabetic by the subcutaneous injection of alloxan monohydrate were found to be resistant to the anorexic action of d-amphetamine. This resistance to amphetamine anorexia did not appear attributable to an increased hunger motivation of the diabetic rats, but rather seemed due to a diminished action of the drug in alloxan-injected animals. This conclusion was supported by further experiments indicating that alloxan-injected rats show diminished locomotor activity and stereotyped behavior following amphetamine administration. Furthermore, the amphetamine resistance appears to be the result of the diabetic state, since amphetamine-induced stereotyped behavior could be reinstated in alloxan-injected rats by the administration of protamine zinc insulin for ten days. The results of these investigations suggest that there exists an altered central nervous system response to d-amphetamine in the diabetic rat. These possibility of an abnormal functioning of central catecholamine-containing neurons in such animals is discussed.
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PMID:Further analysis of the resistance of the diabetic rat to d-amphetamine. 56 33

1 Intracerebroventricular injection of prostanglandin F2alpha (10-40 microgram) decreases food intake in a dose-dependent manner in rats trained to consume their daily total food intake in a 2 h period. 2 This anorexia is also observed in satiated rats, which had ad libitum access to food. 3 The anorectic activity of prostaglandin F2alpha is not modified by changes in the internal environment of the body after food intake, such as increased blood glucose and insulin levels and decreased fatty acid levels, or by the presence or absence of food in the stomach, as is evident from the anorectic activity of prostaglandin F2alpha in partially satiated rats. 4 The anorexia is not due to pain or irritative properties of prostaglandin F2alpha since induction of comparable pain with 3% acetic acid does not affect food intake in rats deprived of food for 22 hours. 5 Anorectic doses of prostaglandin F2alpha when injected intraperitoneally cause hypothermia. 6 The results suggest that the inhibitory activity of prostaglandin F2alpha on food intake is at both peripheral and central sites. 7 Prostaglandin F2alpha-induced anorexia is associated with the behavioural tranquilization that is seen after the ingestion of food.
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PMID:Some observations on the anorectic activity of prostaglandin F2alpha. 89 Feb 8

The role of central dopaminergic mechanisms in the regulation of food and water intake was assessed by examining the effects of haloperidol and pimozide on various measures of feeding and drinking in rats. Haloperidol (0.20 mg/kg) or pimozide (0.45 mg/kg) did not significantly affect 1-hr water intake in response to 24 hrs of water deprivation, nor did they influence 2-hr food intake after 24 hrs food deprivation. However both pimozide and haloperidol significantly reduced drinking in response to injections of hypertonic saline. In addition, animals pretreated with these drugs drank less than controls in the absence of food (a measure of "non-prandial" drinking), and drank less than controls when the water was adulterated with quinine (a measure of "finickiness"). These drugs also significantly reduced food intake in response to injections of insulin and attenuated amphetamine anorexia. These deficits are similar to those observed after electrolytic lesions of the lateral hypothalamus or after 6-hydroxydopamine lesions of the substantia nigra. Because haloperidol and pimozide block central dopaminergic receptor sites, the present findings are consistent with the hypothesis that part of the lateral hypothalamic syndrome is the result of damage to the dopaminergic nigro-neostriatal projection. Finally, the data suggest that the changes in feeding and drinking induced by haloperidol and pimozide reflect genuine homeostatic deficits rather than being due to a neuroleptic-induced motor dysfunction.
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PMID:Neuroleptic-induced deficits in food and water regulation: similarities to the lateral hypothalamic syndrome. 116 94

Many common metastatic cancers are associated with marked weight loss at the time of diagnosis. Anorexia clearly plays a major role in weight loss in the cancer patient, but cannot explain all of the weight loss noted. Malnourished patients with localized cancers under metabolic ward conditions fail to gain weight when given apparently adequate calories for anabolism, thus suggesting that these patients are hypermetabolic. Increased whole body protein breakdown, increased lipolysis, and increased gluconeogenesis have been repeatedly demonstrated in malnourished cancer patients. Protein and glucose metabolism are closely linked, and both are regulated by a number of the same hormones and metabolites. For example, when increased glucose production in malnourished cancer patients is inhibited pharmacologically, protein catabolism is proportionally decreased. Studies of glucose, growth hormone, cortisol, and insulin secretion following an oral glucose load in well-nourished cancer patients are consistent with insulin resistance but no other hormonal abnormalities. Malnourished cancer patients have elevated levels of growth hormone that are further stimulated by arginine and insulin infusion. No abnormalities of thyroid function were noted in cancer patients. Current studies are underway to determine the mechanisms and effects of progestational steroids and cytokines on both food intake and intermediary lipid metabolism.
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PMID:Hormonal and metabolic abnormalities in the malnourished cancer patient: effects on host-tumor interaction. 128 26

Insulin resistance contributes to the metabolic defects in non-insulin-dependent diabetes mellitus (NIDDM). Anorectic agents have been shown to improve insulin action in NIDDM, irrespective of weight reduction. The serotonin-reuptake inhibiting agent fluoxetine has recently been recognized as an anorectic agent. The effect of fluoxetine on insulin action has not yet been determined. In a double blind placebo controlled crossover study, we examined hepatic and peripheral insulin action by the sequential hyperinsulinemic euglycemic clamp technique with infusion of 3-3H-glucose in eight obese NIDDM and in eight obese nondiabetics, matched for age, sex and body mass index. Body weight was kept constant. After 14 days of fluoxetine, 60 mg daily, in NIDDM half-maximal peripheral glucose uptake was achieved at a lower insulin level than after placebo (ED50pgu 180.5 +/- 25.8 vs 225.3 +/- 39.9 mU/l, P less than 0.05), but not in nondiabetics (140 +/- 15.3 vs 135.3 +/- 22.2 mU/l, n.s.). Maximal peripheral glucose uptake (Vmaxpgu) did not change significantly. Basal hepatic glucose production (HGP) was reduced after fluoxetine in both NIDDM (9.45 vs 10.37 mumol/kg/min) and in nondiabetics (8.57 vs 9.16 mumol/kg/min), although the difference was only significant in nondiabetics (P less than 0.05). Multivariate analysis disclosed no differences in the effect of fluoxetine between NIDDM and nondiabetics. When nondiabetics and NIDDM were considered together, only the most insulin-resistant individuals demonstrated a decrease in ED50pgu (P less than 0.001). Likewise, only the individuals with the most outspoken hepatic insulin resistance demonstrated a decrease in insulin level, at which hepatic glucose production is completely suppressed (HGP0) (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluoxetine increases insulin action in obese nondiabetic and in obese non-insulin-dependent diabetic individuals. 131 30

Insulin resistance contributes to the metabolic defects in non-insulin dependent diabetes mellitus (NIDDM). Anorectic agents have been shown to improve insulin action in NIDDM, irrespective of weight reduction. In a double-blind placebo-controlled cross-over study, we examined hepatic and peripheral insulin action by the sequential hyperinsulinaemic-euglycaemic clamp technique with infusion of 3-[3H]-glucose in eight obese NIDDM patients and in eight obese non-diabetics, matched for age, sex and body mass index. Body weight was kept constant. After 14 days of fluoxetine, 60 mg daily, in NIDDM half-maximal peripheral glucose uptake was achieved at a lower insulin level than after placebo (ED50pgu: 180.5 +/- 25.8 vs. 225.3 +/- 39.9 mU/l, P < 0.05), but not in non-diabetics (140 +/- 15.3 vs. 135.3 +/- 22.2 mU/l, n.s.). Maximal peripheral glucose uptake (Vmaxpgu) did not change significantly. Multivariate analysis disclosed no differences in the effect of fluoxetine between NIDDM and non-diabetics. When non-diabetics and NIDDM were considered together, only the most insulin-resistant individuals demonstrated a decrease in ED50pgu (P < 0.001). Likewise, only the individuals with the most outspoken hepatic insulin resistance demonstrated a decrease in insulin level, at which hepatic glucose production (HGP) is completely suppressed (HGP0) (P < 0.01). In conclusion, fluoxetine improves peripheral and hepatic insulin action in obese insulin-resistant subjects irrespective of its weight lowering effect.
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PMID:Fluoxetine increases insulin action in obese type II (non-insulin dependent) diabetic patients. 133 87

Several studies have demonstrated the efficacy of cyclosporin A in modifying the initial course of Type 1 (insulin-dependent) diabetes mellitus in older children and adults but none have reported the effects in very young children. We treated 14 newly-diagnosed Type 1 diabetic patients aged 22 months to 95 months with cyclosporin A. Mean insulin dose at entry was 0.7 +/- 0.07 IU.kg-1.day-1. Initial cyclosporin A dose was 10 mg.kg-1.day-1. Insulin dose reached a nadir of 0.13 IU.kg-1.day-1 by 180 days. Mean glucagon-stimulated connecting peptide levels were maximal at 6 months (0.75 nmol/l) and were maintained while on cyclosporin A. Insulin was discontinued in four patients for 4, 12, 15 and 30 months respectively. In five other patients the insulin dose was less than 0.15 IU.kg-1.day-1 for at least 3 months. Glycated haemoglobin levels for all patients were within the normal range. Side effects included anorexia, stomach pains, poor weight gain, hypertrichosis, gum hyperplasia, mild anaemia and elevated creatinine. All patients have now discontinued cyclosporin A and all but one have been followed for 5 years after discontinuation. Reasons for discontinuing cyclosporin A included exposure to chicken pox (varicella), non-resolving otitis media, incomplete or no response and relapse. All side effects have resolved since the treatment was discontinued. Following discontinuation of cyclosporin A insulin requirements and glycated hemoglobin levels increased while glucagon-stimulated connecting peptide levels declined dramatically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A treatment of young children with newly-diagnosed type 1 (insulin-dependent) diabetes mellitus. London Diabetes Study Group. 139 85

Nearly 50% of individuals with type II diabetes mellitus are over the age of 65 years. There are numerous reasons to maintain blood glucose levels below 11.1 nmol/L (200 mg/dl) in older persons, and there are a number of changes often seen with advancing age that persons, and there are a number of changes often seen with advancing age that may interfere with the management of diabetes mellitus, e.g. hypodipsia, anorexia, visual disturbance, altered renal and hepatic function, depression, impaired basoreceptor response and multiple medications. Hyperglycaemia appears to produce cognitive impairment which may lead to poor compliance. It is often difficult to manipulate diet in older people, and in fact dietary changes can lead to severe protein energy malnutrition. High maximum voluntary oxygen intake has been correlated with increased glucose disposal, but there is little evidence that physical exercise can improve diabetic control in the elderly. Oral sulphonylurea hypoglycaemic agents are extremely useful in the treatment of diabetes in these patients, but it should be remembered that they are more liable to develop hypoglycaemia than are younger diabetics. The role of metformin in the management of older diabetic patients is poorly studied. Many older persons can cope well with insulin therapy, but those with visual disturbances often make errors when drawing up insulin and require special attention. Combination therapy of insulin with oral hypoglycaemic agents is not recommended in this group of patients, and serum fructosamine is preferred to glycated haemoglobin to monitor control. Successful management of elderly diabetic patients thus requires an interdisciplinary team approach.
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PMID:The management of diabetes mellitus in older individuals. 171 59


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