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Insulin release in hyperuricemic patients
No full textThe insulin response to oral glucose and to i.v tolbutamide was stuied in a group of hyperuricemic subjects and in a group of weight-matched controls. Glucose tolerance was impaired only in obese hyperuricemic subjects. Insulin response to oral glucose was enhanced in hyperuricemic subjects. Tolbutamide gave rise to a sharp increase in IRI levels already 2 min after the injection and this rise was significantly higher in hyperuricemic subjects than in controls. The same result was observed also after i.v. fructose. The interpretation of these data is not easy. Uric acid plasma level and obesity do not seem to be directly involved because an abnormal IRI response has been observed also after a rapid fall in uric acid plasma level after allopurinol treatment and is evident also in lean subjects. In our opinion the problem is more complex and must be considered from the point of view of a change involving carbohydrate as well as purine metabolism
The effect of pyridoxine-alpha-ketoglutarate (PAK) on exercise-induced increase of blood lactate in patients with type I diabetes.
No full textAdministration of pyridoxine-alpha-ketoglutarate (PAK) to a group of insulin-independent non-ketotic diabetics decreased (p less than 0.01) the plasma concentration of lactate response to isometric exercise. The mechanism of action of PAK could be interpreted as a consequence of changes induced by the drug on the Krebs' cycle with a subsequent reduction of lactate production
Relationships between insulin secretion, insulin metabolism and insulin resistance in mild glucose intolerance.
No full textThe aim of this study was to evaluate whether the correlation between insulin resistance and peripheral hyperinsulinaemia existing in mild glucose intolerance corresponds to a relationship between insulin resistance and insulin overproduction by the pancreas. In addition, the possibility that insulin resistance is related to insulin metabolism was examined. Twenty five subjects with fasting normoglycaemia and an abnormal glucose response to the oral glucose tolerance test (OGTT) were studied. Insulin secretion by the pancreas was estimated by means of fasting C-peptide levels in peripheral blood. Insulin resistance was estimated by the rate of glucose disappearance from plasma after i.v. insulin injection. Insulin metabolism was estimated indirectly by the C-peptide: insulin molar ratio. A negative correlation was found between the glucose disappearance rate from plasma after i.v. insulin injection and fasting insulin levels (r = -0.677, p less than 0.001), but not fasting C-peptide concentrations (r = -0.164, p = NS). Glucose disappearance rate from plasma correlated positively with the C-peptide: insulin molar ratio (r = 0.626, p less than 0.001). These results suggest that in mild glucose intolerance insulin resistance and insulin secretion by the pancreas are not related phenomena, and that the defect responsible for insulin resistance might also be implicated in the impaired insulin metabolism
[Relations between the blood insulin and sugar response to oral glucos loading in normal subjects and in subclinical and manifest diabetes].
No full textFurther evidence that insulin metabolism is a major determinant of peripheral insulin response to oral glucose in subjects with mild glucose intolerance.
No full textIn mild glucose intolerance plasma concentration of C-peptide seems to give an estimate of pancreatic B cell secretion more reliable than plasma insulin itself. In the present study we measured the plasma levels of insulin and C-peptide after oral glucose load in 100 mildly glucose intolerant subjects, focusing our attention on high and low insulin responders. According to an insulin incremental area after oral glucose higher or lower than the mean +/- SD of the mean, 16 subjects were classified as "high insulin responders", and 17 as "low insulin responders". The two groups were similar for sex, age and bw. Mean insulin incremental area was almost 9-fold greater in high insulin responders than in low insulin responders (0.88 +/- 0.03 vs 0.10 +/- 0.01 pmol/ml min, p less than 0.001). Also mean C-peptide incremental area was significantly greater in high insulin responders than in low insulin responders, but the differences between the two groups were smaller. Indeed, mean C-peptide area was approximately 2.5-fold greater in high insulin responders than in low insulin responders (1.58 +/- 0.12 vs 0.66 +/- 0.07 pmol/ml min, p less than 0.001). These results give further support to the concept that in mild glucose intolerance insulin metabolism is a major determinant of peripheral insulin response to oral glucose load
[Genetic markers in insulin-dependent juvenile diabetes].
No full textA significant association has been established between insulin-dependent diabetes and HL-A. This was appraised in a selected series of 16 patients and 64 of their first-degree relatives by HL-A typing. The relatives also underwent a glucose tolerance test. The results showed a high incidence of B8 in the patients (31%, VS 15% in controls: p less than 0.01). A previously observed prevalence of Bw 15, however, was not noted. In addition, an increased incidence of Bw 35 was detected (38%, VS 23% in the controls: p less than 0.02). In the case of the relatives, no significant differences in HL-A frequency were apparent, nor could a relationship between HL-A phenotype and altered glucose tolerance be established. The true aetiopathogenetic significance of this association is discussed in the light of recent views concerning HL-A and diseases
Decreased hepatic insulin extraction in subjects with mild glucose intolerance.
No full textThe fact that hyperinsulinemia occurs in simple obesity and mild glucose intolerance has been well established. Altered hepatic insulin extraction may influence the levels of circulating hormone. The simultaneous measurement of insulin and C-peptide concentrations in peripheral blood enables an in vivo estimation of hepatic insulin removal. To evaluate hepatic insulin extraction, insulin and C-peptide responses to oral glucose were studied in 176 obese and nonobese subjects with normal, impaired, or diabetic glucose tolerance. Insulin levels as well as insulin incremental areas in glucose intolerant subjects were significantly higher than in weight-matched controls. The levels of C-peptide as well as C-peptide incremental areas were only slightly enhanced in subjects with impaired glucose tolerance, whereas they were reduced in subjects with diabetic tolerance. The molar ratios of C-peptide to insulin, both in the fasting state and after ingestion of glucose, as well as the relationship between the incremental areas of the two peptides were used as measures of hepatic insulin extraction. They were significantly reduced in glucose intolerant subjects and, to a lesser extent, in nondiabetic obese subjects. These results indicate that peripheral hyperinsulinemia in subjects with simple obesity or impaired glucose tolerance is a result of both pancreatic hypersecretion and diminished hepatic insulin extraction. In subjects with a more severe degree of glucose intolerance, decreased hepatic insulin removal is the primary cause of hyperinsulinemia
[Changes induced by various drugs (allopurinol, metformin) in various dysmetabolic components of primary hyperuricemia].
No full textLack of effect of intravenous metformin on plasma concentrations of glucose, insulin, C-peptide, glucagon and growth hormone in non-diabetic subjects.
No full textA study was carried out to evaluate the acute effect of an intravenous injection of metformin on the fasting plasma concentrations of glucose, insulin, C-peptide, glucagon and growth hormone in 15 non-diabetic subjects. Metformin (1 g) was administered as a bolus in a peripheral vein and blood was sampled 2, 5, 10, 15 and 30 minutes after the drug injection. No significant change in fasting concentration of glucose nor in C-peptide, insulin, glucagon and growth hormone fasting levels was noticed. It is concluded that metformin does not possess an acute direct hypoglycaemic effect in non-diabetic subjects and does not acutely affect the basal activity of endocrine pancreas and pituitary gland in releasing insulin, glucagon and growth hormone
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