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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of exercise on forearm muscle metabolism was examined in 9 healthy subjects, in 16 diabetics and in 4 obese subjects during complete starvation. During exercise glucose uptake rose 7-8 fold in the controls. However, no increase of glucose uptake was observed in the other groups studied. Moreover, a glucose production from the working muscle took place in about 40 percent of both the diabetic patients and the starved obese subjects. The nonutilization of glucose during physical work in the diabetic like states was accompanied by a significantly diminished lactate output. The arterial concentration of FFA, glycerol beta-HOB and Acac was markedly elevated in the starved obese patients. The FFA-uptake at rest and during exercise, however, was not different from results of controls. Whereas an effux of beta-HOB has been observed during exercise, Acac uptake was increased in these patients. It is suggested that in maturity onset and starvation diabetes glycolysis is inhibited.
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PMID:Muscle metabolism during exercise in diabetics and in obese during starvation. 68 Jun 26

To evaluate the role of glucagon in the pathogenesis of diabetic ketoacidosis in man, we studied the effect of suppression of glucagon secretion by somatostatin on changes in plasma beta-hydroxybutyrate and glucose concentrations (as well as changes in their precursors) after acute withdrawal of insulin from seven patients with juvenile-type diabetes. Suppression of glucagon secretion prevented the development of ketoacidosis for 18 hours after acute insulin withdrawal, whereas in control studies mild ketoacidosis occurred 10 hours after insulin was stopped. Plasma beta-hydroxybutyrate, glucose, free fatty acid, and glycerol levels were all markedly lower during suppression of glucagon secretion (p smaller than 0.001), whereas plasma alanine levels were higher (p smaller than 0.001). These studies indicate that insulin lack per se does not lead to fulminant diabetic ketoacidosis in man and that glucagon, by means of its gluconeogenic, ketogenic, and lipolytic actions, is a prerequisite to the development of this condition.
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PMID:Prevention of human diabetic ketoacidosis by somatostatin. Evidence for an essential role of glucagon. 80 37

In order to investigate the contribution of glucagon to the abnormalities of carbohydrate and lipid metabolism in diabetes, hormones and metabolites were measured in response to IV arginine in 5 juvenile onset (control) diabetics and 5 totally pancreatectomised subjects. In the basal state, both control diabetics and pancreatectomised patients showed abnormally elevated levels of plasma glucose, blood 3-hydroxybutyrate, glycerol and plasma free fatty acids (NEFA), although no glucagon was detectable in the plasma of the pancreatectomised subjects. Blood concentrations of the gluconeogenic precursors alanine and glycerol were higher pancreatectomised patients than in the diabetics. Following infusion of arginine, the rise in glucagon observed in the diabetics was accompanied by a significant increase in plasma glucose and a fall in blood lactate when compared to the pancreatectomised subjects. In spite of the rise in glucagon in the control diabetics, no sigficant change was found in the concentrations of ketone bodies, glycerol or NEFA. Thus glucagon does not seem to have a primary role in producing the metabolic abnormalities of diabetes.
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PMID:Persistent metabolic abnormalities in diabetes in the absence of glucagon. 83 5

Studies of fat mobilization and transport are reported in six patients with the Prader-Willi syndrome. Two patients had carbohydrate intolerance. One of these had a low and the other an augmented insulin response to glucose challenge. Following challenge with glucose, three of the four nondiabetics had normal insulin responses or increased responses consistent with their obesity; the other nondiabetic had insulinopenia. Measurements of the effects of norepinephrine, insulin, glucose, and 5-methylpyrazole-3-carboxylic acid on plasma levels of FFA, glycerol, and ketones provide no evidence for abnormal regulation of mobilization of fat from adipose tissue. Measurements of plasma lipids and postheparin lipolytic activity are consistent with normal uptake of fat into adipose tissue, and normal fatty acid composition of adipose tissue gives no evidence for abnormal lipogenesis.
Diabetes 1977 Sep
PMID:The Prader-Willi syndrome. Regulation of fat transport. 89 39

In diabetics with different therapy indications the effect of the treatment on the lipid parameters of blood was examined. We estimated the change of the triglycerides, the cholesterol, the free fatty acids and the glycerol depending on the duration of the therapy. We used a combined stimulation test (combination of 100 g glucose, 1.0 g tolbutamide and 1.0 g glucagon in temporary coupling) as method for characterization of the type of diabetes. At the beginning of the therapy the fat parameters mentioned did not differ in patients with exclusively dietetic treatment and in SuH-patients. After longer duration of the therapy in exclusively dietetically compensated patients the fasting glycerol values decreased, were, however, statistically not significant. There were also no essential changes of the triglycerides, the cholesterol and the values of the free fatty acids in the two forms of treatment. The improvement of the carbohydrate tolerance could not be explained with changes of the insulin secretion. The results plead for the fact that the improvement of the diabetic metabolism develops by an increase of the peripheral insulin effectivity. The behaviour of the lipid parameters is not sufficient for an explanation of the carbohydrate tolerance.
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PMID:[Effect of diabetes therapy on the lipid parameters in blood]. 91 May 22

Blood lipids and glucose were studied in streptozotocin diabetic rats during hyperthermia. Blood glucose, free fatty acids (F.F.A.) and glycerol of diabetic rats with a rectal temperature of 42 degrees C (hyperthermic) were elevated significantly above those values found in normothermic (TR = 38 degrees C) diabetic or normothermic non-diabetic rats as well as hyperthermic non-diabetic rats. Streptozotocin diabetes caused an elevation in blood triglycerides of normothermic rats, but this hypertriglyceridemia was depressed in diabetic rats during hyperthermia. As in the case of diabetic animals, hyperthermia also caused a depression in the blood triglycerides of non-diabetic rats. However, unlike in the diabetic animals, the blood F.F.A. of non-diabetic rats were depressed during hyperthermia. Although hyperthermia caused a significant increase in the blood glucose of the diabetic animals, no significant change in blood glucose was shown in the hyperthermic non-diabetic rats. Blood cholesterol did not change significantly in the non-diabetic or diabetic animals during hyperthermia. The blood changes of these "energy substrates" are discussed with respect to their possible role in the extreme sensitivity of diabetics to high environmental temperature and "heat stress".
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PMID:Metabolic effect of high environment temperature on non-diabetic and diabetic rats. 92 47

Glycerol, an effective cerebral dehydrating agent, also has gluconeogenic properties, and can thereby elevate serum glucose to dangerously high levels in predisposed patients treated for cerebral edema. The nonketotic hyperosmolar hyperglycemic state usually occurs in cases of maturity onset diabetes or prediabetes, as in the two elderly patients discussed in this paper. The pathogenesis usually evolves through a constant diabetogenic stress that causes persistent hyperglycemia resulting in the exhaustion of ordinarily adequate insulin stores, ultimately allowing hyperglycemia to progress unchecked to metabolic coma. Precautions to recognize this development should be taken in appropriate patients.
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PMID:Nonkitotoc hyperosmolar hyperglycemia during glycerol therapy for cerebral edema. 94 74

The behaviour of glycaemia, insulinaemia, phosphoraemia, somatotropinaemia,free glycerol and triglyceridaemia was studied in six patients with A.L.S. following sugar load (1 g/Kg) in fasting. The results of glycaemia and insulinaemia were in tune with published data which have pointed to reduced sugar tolerance and reduced insulin secretion in patients with A.L.S. In the present experiments, particularly significant were the phosphoraemia responses. The failure of inorganic phosphorus values to fall after glucose loading suggests that the glycidic intolerance of these patients is related above all to a reduction in functioning muscular mass rather than to insufficient insulin secretion. The reduction in nervous tissue may also be of importance in this sense. In fact, not all biohumoral parameters investigated were similar to those of diabetes because the behaviour of somatotropinaemia, free glycerol and plasma triglycerides was normal. The changed behaviour of phosphorus would thus indicate altered glucose uptake at peripheral tissue level.
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PMID:[Aspects of phosphorus and carbohydrate metabolism in amyotrophic lateral sclerosis]. 99 79

It is supposed that the excess of fatty tissue exerts a diabetogenic effect. In obese subjects changes in the reactivity of the enlarged adipocytes to insulin might play a significant role in the pathogenesis of diabetes. Using the method of Rodbell in our own modification the responses of isolated adipocytes obtained from 10 lean and 15 obese subjects to a) insulin, b) theophylline and c) insulin and theophylline jointly (metabolism of glucose and glycerol) were determined. The dose-effect relationship curve was plotted against the effect of glucose utilization caused by increasing concentrations of insulin in the suspensions of adipocytes of lean and obese subjects. In adipocyte donors insulin sensitivity was also determined by Himsworth's test. It was found that adipocytes of 15 subjects with hyperthrophic obesity showed a significantly decreased effect of insulin regulating glucose utilization and glycerol release. They maintained a normal pattern of response to theophylline. The curve of relationship between insulin concentration in the incubation medium and its effect on glucose utilization by the adipocytes was changed. The adipocytes of these donors were relatively refractory to insulin in vivo as determined by the test of Himsworth. The cause of these disturbances may lie in the changed function of insulin receptors in the enlarged adipocytes. The observed disturbances may play a significant role in the pathophysiology of the diabetogenic effect of obesity.
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PMID:Role of disturbed metabolism of fat tissue cells in the pathogenesis of the diabetogenic effect of obesity in humans. 99 68

To evaluate the role of splanchnic and peripheral tissues in the disposal of an oral glucose load, splanchnic exchange of glucose, lactate, pyruvate, glycerol and amino acids was determined in ten healthy subjects in the basal state and for three hours following the oral ingestion of 100 gm. of glucose. Following glucose ingestion, splanchnic glucose output rose rapidly, reaching values two to three times the basal rate at fifteen minutes and returning to baseline by ninety minutes. A secondary rise in splanchnic glucose output occurred at 150 minutes and coincided with a secondary increment in arterial glucose. Total splanchnic glucose output over three hours was 40 plus or minus 3 gm., representing a total increase of only 15 plus or minus 3 gm. above basal splanchnic glucose output. The peak rise in blood glucose was directly proportional to the increase in splanchnic glucose output. Arterial concentrations of alanine, lactate and pyruvate rose by 15, 65 and 80 per cent, respectively, following oral glucose. These arterial elevations were preceded by a 75-100 per cent inhibition of splanchnic uptake of alanine and lactate; in the case of pyruvate there was a reversal from a net uptake in the basal state to a significant net splanchnic output after glucose ingestion. Arterial glycerol fell by 50 per cent and was accompanied by a comparable fall in splanchnic uptake. It is concluded that in normal, postabsorptive man, (a) the major portion of a 100 gm. oral glucose load is retained within the splanchnic bed; (b) only 15 per cent of the ingested glucose is available for disposal by peripheral tissues as increased (above-basal) glucose utilization; (c) the height and shape or the oral glucose tolerance curve are largely determined by the rate and pattern of splanchnic glucose escape; (d) glucose-induced hyperlactatemia, hyperpyruvicemia and hyperalaninemia are due at least in part, to altered splanchnic exchange of these substrates.
Diabetes 1975 May
PMID:Influence of oral glucose ingestion on splanchnic glucose and gluconeogenic substrate metabolism in man. 112 90


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