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Biomedical subjects

A Ramachandran

Publications and source records attributed to A Ramachandran.

At least 181 records · Page 10Linked to original sources
PubMed1988

HLA-D region RFLPs indicate that susceptibility to insulin-dependent diabetes in South India is located in the HLA-DQ region.

Recently close markers for insulin-dependent diabetes mellitus in Western 'Caucasoid' subjects have been defined from DQ region (both alpha and beta genes) restriction fragment length polymorphisms. In order to define the genetic contribution to insulin-dependent diabetes mellitus in an Indian population we have analysed 58 unrelated Dravidian (South Indian) insulin-dependent diabetic patients and 43 controls. In insulin-dependent diabetes an increased frequency of the Taq 1 DQ beta restriction fragment length polymorphisms designated T2 omega/T6 (relative risk = 10.6), and of homozygotes for Taq 1 DQ alpha 4.6 kb (relative risk = 11), was found in the patients. The highest relative risk for insulin-dependent diabetes mellitus was obtained by comparing patients and control subjects who either (a) co-inherited DQT2 omega/T6 with certain DQ alpha restriction fragment length polymorphisms or (b) were DQ alpha 4.6 kb homozygotes, the combination of (a) and (b) accounting for 55.5% of insulin-dependent diabetes mellitus subjects and none of the controls (relative risk = 101; 95% confidence limits 93-109).

Diabetes Mellitus, Type 1↗
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

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

Altered tissue oxygen tension responsiveness in diabetes.

Subcutaneous oxygen tension (tissue PO2) was measured by a polarographic method in the legs of insulin-dependent diabetics (IDDM) and controls. Current flow was measured continuously using a five-stage protocol: baseline; 4 min of complete arterial occlusion; during recovery from ischemia; baseline approximately re-established; induction of hyperemia by local application of heat. Eleven patients with IDDM of 4-32 years of duration, without peripheral arterial disease, were studied and compared with 10 controls. The mean baseline subcutaneous PO2 in diabetics was less than controls; however, the difference was not statistically significant. At the end of arterial occlusion the mean decrease in tissue PO2 was less (P less than 0.025) in diabetics (4.7 +/- 0.9 mm Hg, SEM) compared to controls (10.2 +/- 1.6 mm Hg). With induction of hyperemia the increase in tissue PO2 was lower (P less than 0.001) in diabetics (7.4 +/- 0.4 mm Hg) than in controls (18.6 +/- 1.7 mm Hg). The observed differences provide for the first time direct evidence of altered tissue PO2 responses in diabetes.

Adolescent↗
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↗