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Biomedical subjects

V Mohan

Publications and source records attributed to V Mohan.

At least 217 records · Page 12Linked to original sources
PubMed1987

Changes in plasma growth hormone in diabetic and nondiabetic subjects during the glucose clamp.

A group of 22 newly diagnosed noninsulin-dependent diabetic subjects and seven nondiabetic subjects underwent a glucose clamp at plasma glucose 100 mg/dL with insulin infusion rates of 1.0 and 10 mU/kg/min. During both insulin infusion rates, there was a sustained rise in plasma growth hormone (GH) above basal in 18 of the 22 diabetic subjects. Basal GH values were 2.37 +/- 0.67 ng/mL, rising above basal during the lower insulin infusion (6.1 +/- 3.3 ng/mL, P = 0.05) with a further rise at the higher insulin level (8.58 +/- 2.0 ng/mL, P less than 0.001). There was no rise in GH in any of the nondiabetic subjects. In neither group was there any rise above basal in cortisol, prolactin, glucagon, or somatostatin (SRIH). In a group of three nondiabetic subjects, a rise in GH similar to that seen in the diabetic group was induced by elevating the plasma glucose to 200 mg/dL for 60 minutes prior to the euglycemic clamp procedure. However, it is unlikely that changes in plasma glucose account totally for the changes in plasma GH described in the diabetic subjects since a rise in plasma GH was also seen in four diabetic subjects clamped at their fasting plasma glucose. We conclude that in newly diagnosed noninsulin-dependent diabetic subjects there is a rise in plasma GH during the euglycemic clamp procedure, which may be due to both the prior lowering of plasma glucose and the high plasma insulin levels.

Adult↗
PubMed1987

HLA-DR and -DQ DNA genotyping in insulin-dependent diabetes patients in South India.

Restriction fragment length polymorphisms (RFLPs) of the HLA-DR beta, -DQ alpha, -DQ beta, and -DX alpha genes have been examined in South Indian diabetic patients and controls. The DR. DQ linkage arrangements in South Indians were shown to be different for DR2, DR4, and DRw6 from those commonly seen in Europeans, so that localization of the primary disease-promoting gene in IDDM could be attempted. This study clearly implicates at least one DQ beta allele in the pathogenesis of IDDM.

DNA Probes, HLA↗
PubMed1987

Insulin resistance in maturity onset diabetes of the young.

Insulin resistance was assessed by euglycaemic clamp studies in matched groups of MODY, classical NIDDM patients and non-diabetic control subjects. The MODY patients metabolised less glucose (4.8 +/- 0.3 mg/Kg/min) than the classical NIDDM patients (7.0 +/- 0.5 mg/Kg/min) at an insulin infusion rate of 1.0 mU/Kg/min (p less than 0.05). At an insulin infusion rate 10 mU/Kg/min the differences between the MODY and the classical NIDDM patients were not significant. At both infusion rates the two diabetic groups metabolised less glucose than the control subjects. The results indicate that despite their younger age, the patients with MODY are more insulin resistant than the patients with classical NIDDM.

Adult↗
PubMed1987

Pancreatic beta cell response in insulin treated NIDDM patients limitations of a random C-peptide measurement.

Pancreatic beta cell function was evaluated in 30 insulin treated non-insulin dependent diabetic patients, by estimating serum C-peptide after meal stimulation. C-peptide response was low (less than 0.6 pmol/ml) in 15 patients and it was significant (greater than 0.6 pmol/ml) in the other 15 patients. All the patients were then started on a high carbohydrate, high fibre diet and a combination of glibenclamide and metformin. In 18 patients, optimal regulation of hyperglycemia was achieved in one week and the others required insulin treatment. Among the 15 with low C-peptide values, 8 patients responded to oral hypoglycaemic agents and their C-peptide responses improved (from 0.17 +/- 0.16 to 0.78 +/- 0.2 pmol/ml). Among the 15 with significant C-peptide values, 10 responded well to oral drugs and their C-peptide values improved further (from 0.79 +/- 0.21 to 1.17 +/- 0.44 pmol/ml); but the others required insulin despite the good beta cell reserve. This study shows that the beta cell response in insulin treated NIDDM varies widely as it is influenced by the exogenous insulin and hyperglycaemia a random estimation of C-peptide will be of limited value in predicting the response to therapy.

Adolescent↗