Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetes and carbohydrate intolerance can occur in pancreatitis. Although one-half of patients with acute pancreatitis will have some evidence of glucose intolerance during their acute illness, few will require insulin administration on either a short- or long-term basis. The diabetes seen in acute pancreatitis is likely due to a combination of factors, including alerted insulin secretion, increased glucagon release, and decreased glucose utilization by the liver and peripheral tissue. Chronic pancreatitis is often associated with diabetes mellitus, with the incidence as high as 70 percent when pancreatic calcification is present. These patients tend to be very sensitive to the effects of insulin and hypoglycemia. This is probably secondary to concurrent hepatic disease, malnutrition, and a relative decrease in glucagon reserves. The diabetes seen in chronic pancreatitis is associated with decreased insulin production. Finally, although the endocrine pancreas may influence the exocrine gland through a portal system, primary diabetes mellitus probably does not result in clinically significant alterations in pancreatic exocrine function.
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PMID:Diabetes mellitus and the exocrine pancreas. 636 37

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

The blood levels of amino acids, ammonia and pancreatic hormones following the intragastric and intravenous administration of a branched-chain amino acid (BCAA)-enriched solution were comparatively investigated in control subjects and patients with liver cirrhosis. There was no essential difference in the time course of serum amino acid and blood ammonia levels between the intragastric and intravenous infusions. Elevation of serum insulin concentrations in cirrhotic patients was significant only immediately after the administration through the enteral route. However, plasma glucagon levels increased similarly when the BCAA-enriched solution was administered through either route. The results indicate that both enteral and intravenous infusions will have similar therapeutic effects on the impaired protein metabolism in cirrhotic patients with protein-calorie malnutrition.
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PMID:Comparative study of amino acid, ammonia and pancreatic hormone levels in the blood of cirrhotic patients following intragastric and intravenous administration of a branched-chain amino acid-enriched solution. 641 80

Eleven patients after total pancreatectomy and 68 patients after pancreatoduodenectomy were reviewed for evaluating the importance of nutritional management after massive resection of the pancreas. Nutritional supply by IVH resulted in maintaining and improving the hepatic function under obstructive jaundice in clinical and experimental studies. Administration of elemental diet after the operation shortened the period of IVH, and had a effect to spare the requirement of exogenous insulin. One of the most important problems after pancreatectomy with extensive dissection of the lymph nodes and the nerves around superior mesenteric artery was a malnutrition which appeared frequently after long term follow-up. The malnutrition should be treated by IVH as soon as possible for preventing further aggravation of digestive and absorptive function of the alimentary tract. Oral or nasogastric tube administration of elemental diet is useful for weaning the patient from IVH, and it serves to prevent subsequent development of malnutrition. In six totally pancreatectomized patients studied, postabsorptive plasma concentration of Arg., Lys., Thr., Ala., Gly., Ser. and Pro. were greatly elevated compared to normal value, however these abnormalities were normalized by 1 to 3 mg of glucagon administration. Glucagon administration resulted in no significant change in daily nitrogen balance.
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PMID:[Nutritional management after massive resection of the pancreas]. 643 88

Twenty-seven otherwise healthy patients with localized sarcoma were examined to determine if glucose intolerance can be detected before the appearance of clinical signs of cachexia. No patient had lost weight or demonstrated severe malnutrition. Fasting plasma samples for glucose, insulin, glucagon, and free fatty acids (FFA) were obtained, and a standard intravenous glucose tolerance test performed. Glucose disappearance rate (K) was calculated between 5 and 60 minutes. K levels were compared to those of normal controls and to those of patients with more extensive cancer (statistics obtained from the literature). Levels for K were compared to tumor volume measurements following surgery. Fasting glucose, insulin, and glucagon levels were normal. Fasting FFA levels were slightly elevated. K levels for sarcoma patients were significantly lower than in control patients (P = 0.04), and higher than in patients with advanced cancer (P less than 0.0001). The subset of patients who weighed less than the ideal had a significantly lower K level than did the rest of the sarcoma population. K levels correlated inversely with tumor volume (r = -0.34; P = 0.04). These data indicate that mild glucose intolerance (reduction in clearance of a glucose load) occurs early in untreated sarcoma patients, is most prevalent in patients who maintain less than the ideal weight, correlates with tumor burden, and occurs before other signs of cachexia appear.
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PMID:Glucose intolerance in sarcoma patients. 649 76

Fasting pancreatic glucagon was observed in Jamaican infants during malnutrition and subsequent recovery. Rehabilitation in two groups of children with isocaloric diets rich either in carbohydrate or fat produced no differences in the rate of weight gain. During malnutrition, plasma pancreatic glucagon concentration was 104 +/- 11 (n = 20) pg/ml (mean +/- S.E.) significantly lower than during recovery when the maximum value was 180 +/- 24 (n = 13) pg/ml during the later recovery phase. After clinical recovery glucagon levels declined to 127 +/- 13 (n = 15) pg/ml. Plasma insulin followed a similar pattern, increasing significantly during catch-up growth and declining after recovery. Slower rates of growth were associated with the simultaneous decline in the concentrations of both hormones after clinical recovery.
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PMID:Fasting pancreatic glucagon in Jamaican children during malnutrition and subsequent recovery. 681 14

The influence of a maternal dietary deficiency of zinc, or food restriction on the content and in vitro secretion of pancreatic hormones was measured in rat fetuses on day 19 of gestation. Pregnant Sprague-Dawley rats were fed a zinc-deficient diet (0.4 +/- 0.1 ppm zinc) ad libitum or a zinc-supplemented control diet (100 ppm zinc) either ad libitum or with restricted intake. The insulin content of the fetal pancreas was lower in fetuses from rats subjected to zinc deprivation or to food restriction than in controls. The lower insulin content of fetal pancreata from zinc-deficient rats was related to a lower than normal proportion of insulin-containing beta cells. The lower insulin content of fetal pancreata from rats subjected to food restriction was related to a less than normal amount of insulin per beta cell. Glucagon concentration in the fetal pancreas was lower than normal in response to zinc deficiency but not to food restriction. Fetal hormone release in vitro was also influenced by the maternal diet. The rate of insulin secretion in vitro was normal in fetuses from zinc-deficient rats, but was accelerated in those from females subjected to calorie restriction. The rate of glucagon secretion in vitro was lower than normal in the pancreata of zinc-deficient fetuses. We conclude that insulin and glucagon levels in the fetus were affected by maternal zinc deficiency and, to a lesser extent, by calorie restriction.
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PMID:Effect of maternal zinc deficiency of food restriction on rat fetal pancreas. 2. Insulin and glucagon. 701 96

Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine-induced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway.
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PMID:The endocrine pancreas in pyridoxine deficient rats. 703 87

Male Sprague-Dawley rats (initial weight 400 g) were fed a 0.5% lactalbumin diet containing required amounts of all other known essential nutrients for 14 weeks. The body weights averaged 250 g after depletion when the animals were randomly assigned to four groups of four or five. Rats of one group were killed for baseline analyses on day 0 of repletion. The remaining three groups were repleted for 14 days with a complete L-amino acid diet containing 20% protein equivalent and 0, 0.75 or 1.5% Arg . HCl. Daily feed intakes averaged 11, 15 and 17 g and daily weight gains were 3.3, 7.4 and 8.3 g, respectively. Average values for corresponding groups were: nitrogen balance--116, 187 and 190 mg/day; urinary orotate--4.6, 0.8 and 0.15 mg/day; carcass lipid--27, 37 and 40 g/100 g dry matter. Liver weights per 100 g body weight for 0 arginine exceeded other groups by 40%. There were no differences in creatinine index, nor in plasma concentrations of insulin, glucagon and albumin. The maximal rate of recovery from protein-calorie malnutrition of mature rats required an exogenous source of arginine. Urinary orotic acid excretion provided a reliable measure for determining when arginine needs for maximal rate of repletion were not met.
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PMID:Arginine requirement of mature protein-malnourished rats for maximal rate of repletion. 726 76

Chronic liver disease is characterized by numerous metabolic alterations, predominantly catabolic, resulting in the clinical picture of malnutrition and even cachexia in some patients. The following review focuses on disturbances of glucose metabolism and of hormonal interactions that could contribute to the clinical picture of malnutrition seen in chronic liver disease. Body composition is altered in a characteristic manner with an increase in fat mass and a significant loss of muscle tissue. Furthermore, defective glucose storage due to reduced insulin sensitivity predominantly of muscle tissue has been observed. The pathogenesis of insulin resistance leading to an impaired glucose tolerance or a manifest diabetes mellitus is as yet unknown. A receptor/postreceptor dysfunction probably exists in chronic liver disease that might be explained by the following factors: 1. Altered membrane lipid composition and increased levels of free fatty acids; 2. long-lasting hyperinsulinemia; 3. increased plasma levels of insulin counteracting hormones such as growth hormone, glucagon, catecholamines and possibly cytokines; 4. a lack of liver-derived humoral factors with insulin-like activity, i.e. insulin-like growth factors I and II.
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PMID:Glucose metabolism and liver cirrhosis. 755 77


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