PubMed Health⌕ Search

Biomedical subjects

S Suresh

Publications and source records attributed to S Suresh.

7 recordsLinked to original sources
PubMed1989

The genetic predisposition to fibrocalculous pancreatic diabetes.

Fibrocalculous pancreatic diabetes (previously known as tropical pancreatic diabetes) is a rare cause of diabetes confined to countries within the tropical belt. The aetiology of fibrocalculous pancreatic diabetes is thought to be environmental although the agent(s) is unknown. We have investigated a possible genetic basis of this disease by looking for restriction fragment length polymorphisms of genes implicated in the aetiology of diabetes mellitus. Seventy-six Dravidian patients with fibrocalculous pancreatic diabetes were studied, and the restriction fragment length polymorphisms obtained compared to racially matched control subjects (n = 94), patients with Type 2 (non-insulin-dependent) diabetes (n = 87) and Type 1 (insulin-dependent) diabetes (n = 58). No association of fibrocalculous pancreatic diabetes was found with restriction fragment length polymorphisms of the insulin receptor gene. Although no association of fibrocalculous pancreatic diabetes was found with polymorphism of the HLA DR alpha/DQ alpha/DX alpha genes, an association was found with the Taq 1 restriction fragment length polymorphisms of the DQ beta gene (DQ beta T2/T6 present in 39% of patients with fibrocalculous pancreatic diabetes compared to 19% in control subjects; p = 0.01; corrected p value = 0.04) which is similar to that found in Type 1 but not Type 2 diabetes. An association of fibrocalculous pancreatic diabetes was also found with the hypervariable region in the 5-prime flanking region of the insulin gene; 40% of patients possessed the class 3 allele compared to 9.5% of control subjects p = 0.0001; corrected p value = 0.0008).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Familial aggregation in tropical fibrocalculous pancreatic diabetes.

There is very little information on the genetic factors associated with fibrocalculous pancreatic diabetes (FCPD). Ninety-eight first-degree relatives of FCPD patients were subjected to detailed studies, which included glucose tolerance tests, x-ray films of the abdomen, ultrasonography, and studies of exocrine pancreatic function. The study shows that there is a familial aggregation of FCPD with evidence of vertical transmission of the disease from parent to offspring in some families. Routine screening of families of FCPD probands helped to pick up cases in the stage of impaired glucose tolerance. There is heterogeneity in FCPD with respect to familial factors. Some families show marked familial aggregation of FCPD while in others the disease occurs either sporadically or in association with other family members who have abnormal glucose handling.

Adolescent↗
PubMed1989

Fibrocalculous pancreatic diabetes in the elderly.

Fibrocalculous pancreatic diabetes (FCPD) is a form of diabetes seen in tropical countries. It is secondary to chronic, calcific, non-alcoholic pancreatitis. FCPD is usually a disease of youth. This paper reports on two elderly onset cases of FCPD. Macrovascular complications are usually rare in FCPD patients. These two patients had evidence of macrovascular diseases probably due to the older age group of the patients.

Calcinosis↗
PubMed1986

Effect of insulin on low-density-lipoprotein metabolism in human lymphocytes in vitro.

The metabolism of low-density lipoproteins (LDL) in vitro in the presence of insulin was studied in freshly isolated human peripheral-blood lymphocytes. Insulin appeared to decrease the binding affinity of 125I-LDL to its cell-surface receptor, without any change in apparent Vmax or in the number of LDL receptors. As a consequence, the absolute amounts of 125I-LDL internalized and degraded were lower in the presence of insulin than in its abscence, although the fraction of internalized 125I-LDL degraded in either instance was quite similar. 3-Hydroxy-3-methylglutaryl-CoA reductase activity, and hence cholesterol synthesis, were stimulated by insulin. This effect of insulin was independent of the inhibitory effect of LDL on cholesterol synthesis. At the same time, acid cholesterol esterase and acyl-CoA: cholesterol O-acetyltransferase activities were lower in cells incubated with insulin than in controls. The net effect of these metabolic alterations seems to be that cells accumulate greater quantities of free and esterified cholesterol when treated with insulin.

AMP-Activated Protein Kinases↗