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Biomedical subjects

V Mohan

Publications and source records attributed to V Mohan.

At least 127 records · Page 7Linked to original sources
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↗
PubMed1986

Serum immunoreactive insulin responses to a glucose load in Asian Indian and European type 2 (non-insulin-dependent) diabetic patients and control subjects.

The serum immunoreactive insulin response to an oral glucose load was estimated in 15 Asian Indian and 29 European non-diabetic subjects, and in 45 Asian Indian and 72 European Type 2 (non-insulin-dependent) diabetic patients. In the non-diabetic group, basal insulin values were higher in the Asian Indians than the Europeans (16.7 +/- 3.0 vs. 6.9 +/- 0.7 mU/l, p less than 0.001), and remained higher throughout the glucose tolerance test. Total insulin response was also higher in the Asian Indians (p less than 0.001), and linear regression analysis revealed basal insulin, body mass index and race to be important predictors of insulin response. Amongst the diabetic patients, basal insulin values were again higher in the Asian Indians compared with the Europeans (18.0 +/- 5.0 vs. 11.5 +/- 0.9 mU/l, p less than 0.05). Total insulin response was also greater (p less than 0.01). Linear regression analysis revealed the basal insulin value to be the only significant predictor of insulin response. The results demonstrate higher insulin levels in Asian Indians than Europeans in both normal subjects and Type 2 diabetic subjects. The insulin response to a glucose load is also greater in the Asian Indians. In the control subjects, ethnic differences contribute to this response, whereas in the diabetic patients this is a function of the elevated basal insulin values of the Asian Indians.

Adult↗
PubMed1986

Significance of impaired glucose tolerance in an Asian Indian population: a follow-up study.

A prospective study was undertaken in 107 Indians with impaired glucose tolerance (IGT) for a period ranging from 2 to 10 years. On follow-up, 32% still had an impaired glucose tolerance, 32% reverted to normal glucose tolerance and 36% developed diabetes. Careful dietary adherence and weight reduction were found to favour normalisation of glucose tolerance. Poor dietary adherence, persistent obesity and weight gain were found to precipitate diabetes. The study stresses the need for intensive diet therapy in individuals with IGT. Insulin responses were heterogeneous in IGT and non-predictive of the follow-up changes in glucose tolerance.

Adult↗
PubMed1986

Beta cell function in long term NIDDM (type 2) patients and its relation to treatment.

Pancreatic beta cell function was assessed by estimation of fasting and post prandial plasma C-peptide in 183 non-insulin dependent diabetic patients, who were treated with oral hypoglycaemic drugs, for more than 10 years. One-hundred-and-forty-one patients, continued to respond to oral hypoglycaemic agents (Group I) and in 42 the control was not satisfactory and had to be changed over to insulin (secondary failure, Group II). Significant beta cell reserve (PP CP greater than or equal to 0.6 pmol/ml) was present in 89 out of 183 patients (48%) and 83 (93%) of them responded to oral hypoglycaemic agents. Among the 94 patients with low beta cell reserve, 58 (62%) were on oral hypoglycaemic agents and the other 36 (38%) were on insulin. Of the 42 patients with secondary failure to the oral drugs, 36 (86%) had low C-peptide while 6 (14%) had significant C-peptide values. Secondary failure to oral hypoglycaemic agents can also occur in spite of good beta cell reserve. Beta cell reserve was not correlated either to the duration of diabetes or the age at diagnosis of the patients.

Administration, Oral↗
PubMed1986

Insulin response in obese and nonobese offspring of conjugal Indian diabetic parents with increasing glucose intolerance.

Pancreatic beta cell function in response to glucose was assessed in three different groups of offspring of conjugal diabetic parents (OCDP): those with normal glucose tolerance, those with impaired glucose tolerance (IGT), and those with diabetes. Serum immunoreactive insulin (IRI), C-peptide (CP), insulin/glucose (I/G) ratio, and IRI/CP ratios were estimated at fasting and 90 min after glucose load. Insulin secretion, measured as CP, was found to be low even in normal nonobese OCDP, but the change was not reflected in IRI value as the IRI/CP ratio was found to be elevated. The values decreased with increasing glucose intolerance. In obese OCDP, all the parameters were abnormal even among those with normal glucose tolerance, and further deterioration occurred with increasing glucose intolerance. The study shows that insulin secretory defects are detectable even in normal OCDP, and these changes deteriorate with increasing glucose intolerance. Differences are noted in the peripheral concentrations of IRI and CP between obese and nonobese OCDP before development of diabetes. After development of diabetes mellitus, these differences disappear, and the CP and IRI values in both groups are similar and low.

Adult↗
PubMed1986

Beta cell function in insulin-treated non-insulin-dependent diabetic patients.

Non--insulin-dependent diabetes mellitus (NIDDM) patients, 94 in number, who were treated with insulin for various reasons for periods ranging from 2 to 10 years, were investigated to study the effect of long-term insulin therapy and also the effect of anti-insulin antibodies on the beta cell function. Insulin antibody titer and the stimulated C-peptide (CP) did not correlate with the duration of insulin therapy, dose of insulin, or the severity of hyperglycemia. The antibody titers were low in 45%, moderate in 10%, and high in 45%; no correlation was found between the antibody titers and the CP values. Satisfactory control of hyperglycemia was obtained in 54 patients after change of treatment to oral hypoglycaemic agents (OHA). The other 40 patients required continued insulin therapy. The initial CP values were similar in both the groups before initiating the new therapeutic patterns. Those who responded to OHA showed improved CP values on follow-up. The beta cell response to exogenous insulin is heterogeneous in NIDDM patients. In many patients, adequate preservation of beta cell function is present even after long-term insulin therapy. Many of them respond to OHA. Insulin antibodies do not influence the secretory status of the beta cells in NIDDM patients.

Adult↗