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Biomedical subjects

C Snehalatha

Publications and source records attributed to C Snehalatha.

At least 145 records · Page 8Linked to original sources
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

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↗
PubMed1985

Tropical pancreatic diabetes in South India: heterogeneity in clinical and biochemical profile.

Clinical and biochemical studies were carried out in 33 patients with diabetes secondary to chronic calcific, non-alcoholic pancreatitis (tropical pancreatic diabetes) and in 35 Type 2 (non-insulin-dependent) diabetic patients and 35 non-diabetic subjects. Despite lower body mass indices, only 25% of patients with tropical pancreatic diabetes had clinical evidence of malnutrition. There was no history of cassava ingestion. Mean serum cholesterol concentration was significantly lower in the tropical pancreatic diabetic patients (p less than 0.01) in comparison with the Type 2 diabetic patients or non-diabetic subjects, due to a significantly decreased concentration of LDL cholesterol (p less than 0.01) and VLDL cholesterol (p less than 0.05). Basal and post-glucose stimulated concentrations of serum C-peptide were highest in those pancreatic diabetic patients (n = 11) who responded to oral hypoglycaemic drugs, intermediate in the majority (n = 17), who were insulin dependent and ketosis resistant and negligible in a small sub-group (n = 5) who were ketosis prone. The occurrence of microangiopathy in pancreatic diabetic patients was common and similar to that in Type 2 diabetic patients. Thus, tropical pancreatic diabetes in South India appears to be heterogeneous with respect to level of nutrition, severity of glucose intolerance, B-cell function, response to therapy and the occurrence of microvascular complications.

C-Peptide↗
PubMed1985

High prevalence of type 2 (non-insulin-dependent) diabetes among the offspring of conjugal type 2 diabetic parents in India.

The prevalence of Type 2 (non-insulin-dependent) diabetes among offspring of conjugal Type 2 diabetic parents in India was determined by performing oral glucose tolerance tests. Diabetes was present in 50% of offspring, and 12% had impaired glucose tolerance according to the National Diabetes Data Group criteria. Thus, 62% of all offspring had abnormal glucose tolerance tests. This is the highest prevalence rate for diabetes among offspring of conjugal diabetic parents and might represent an ethnic variation of the genetic factors operating in Indian patients with Type 2 (non-insulin-dependent) diabetes.

Adult↗
PubMed1985

HLA, complement C2, C4, properdin factor B and glyoxalase types in South Indian diabetics.

A series of diabetic patients from 3 centres in South India have been tested for HLA A, HLA B, BF, C2, C4A, C4B and GLO types. For insulin-dependent diabetes mellitus (IDDM) patients there was a significant increase in HLA B8, of BF F and decrease of C4 A6. No significant variation in HLA, BF, C2 or GLO frequencies was found in non-insulin-dependent diabetes mellitus (NIDDM) patients, but there was a significant decrease in C4B 1 and an increase in C4B 2. The HLA and BF association in South Indian IDDM patients is very different from that reported previously in North India.

Adolescent↗
PubMed1985

Insulin and C-peptide responses to glucose load in cystic fibrosis.

Immunoreactive Insulin and C-peptide responses to glucose load were estimated in patients with cystic fibrosis and in controls. Both insulin and C-peptide responses were low in cystic fibrosis patients and the changes were more marked in those with glucose intolerance. There appears to be true pancreatic hyposecretion of insulin in patients with cystic fibrosis whereas the peripheral sensitivity of insulin seems to be normal or enhanced.

Adolescent↗
PubMed1984

Serum uric acid concentrations in offspring of conjugal diabetic parents.

Serum uric acid concentrations were measured in offspring of conjugal diabetic parents, in diabetic patients, and in matched nondiabetic controls. The mean uric acid level in offspring of conjugal diabetic parents was significantly higher than in the controls and diabetic patients (P less than 0.001 in the nonobese and P less than 0.05 in the obese). Diabetic patients did not show significant differences in the serum uric acid concentration compared to the controls. The elevated level of serum uric acid in offspring of conjugal diabetic parents could possibly be an early biochemical marker of diabetes.

Adult↗
PubMed1984

Pancreatic beta cell function in offspring of conjugal diabetic parents. Assessment by IRI and C-peptide ratio.

Serum C-peptide and insulin responses to oral glucose load were measured in 69 offspring of conjugal diabetic parents (OCDP). The insulin responses were varied. The non obese OCDP showed higher mean insulin levels than non obese controls while the obese OCDP did not have significant differences in the mean insulin responses compared to obese controls. The C-peptide levels were, however, low in both obese and non-obese OCDP. The IRI/CP ratios were elevated in both groups of OCDP. These results suggest that OCDP have low beta cell function and also possibly a change in the metabolism of insulin at the hepatic level, which is more pronounced in non obese OCDP.

Adolescent↗
PubMed1984

Hepatic extraction of insulin in non-insulin dependent diabetes. Comparative study of obese and non-obese patients.

Changes in the secretion and metabolism of insulin were measured by estimating serum C-peptide and insulin and their ratio during oral GTT in 30 non obese and 12 obese NIDDM patients. The mean IRI and CP responses were low in both groups of patients, compared to weight-matched controls. The reduction in CP was more marked than the reduction in IRI. The molar ratio of insulin and CP was found to be elevated in the patients, probably indicating reduced hepatic and peripheral extraction of insulin. It was noted that the elevated IRI/CP ratio was a 1) a common feature in NIDDM, irrespective of the body weight, 2) it is present even under basal conditions when the insulin levels are the lowest, 3) it appears to be independent of the concentration of insulin reaching the liver, and 4) obese patients appear to have an exaggerated defect compared to their non obese counterparts.

Adult↗
PubMed1983

Pancreatic beta-cell function in tropical pancreatic diabetes.

Individuals with tropical pancreatic diabetes (TPD) have features of malnutrition and insulin-dependent diabetes but do not exhibit ketosis on withdrawal of insulin. Fasting and postglucose C-peptide responses were assessed in TPD and compared with noninsulin-dependent (NIDDM), insulin-dependent (IDDM), and control groups, matched for body weight. The C-peptide concentrations were lower in TPD in comparison with the controls and NIDDM patients but were significantly higher than in classical IDDM. It is likely that the higher C-peptide is responsible for the ketosis resistance in these patients.

Adolescent↗