12
Views
5
CrossRef citations to date
0
Altmetric
Research Article

Low Bodyweight Type 2 Diabetes Mellitus

Pages 229-239 | Published online: 13 Jul 2009
 

Abstract

Non-insulin dependent diabetes mellitus (NIDDM) is the most prevalent form of diabetes mellitus (DM) in India. Currently the nomenclature is Type 2 diabetes mellitus (Type 2 DM). About one fourth of these diabetics have a body mass index (BMI) below 19, i.e. low bodyweight Type 2 DM (LB Type 2 DM). They are neither protein deficient nor belong to a poor socio-economic class. LB Type 2 DM more often presents with peripheral neuropathy and infections than coronary artery disease (CAD), hypertension or nephropathy. They achieve good glycemic control with sulphonylurea therapy. The leading causes of death are infection, coma, renal failure and cerebrovascular accident. LB Type 2 DM patients have severe basal hyperglycemia with low circulating levels of insulin while C-peptide levels are similar to those of patients with classic Type 2 DM. Studies on hepatic glucokinase levels and hepatic-microsomal enzyme systems (mixed function oxidase and cytochrome P450) using antipyrine and lidocaine as in vivo probes revealed hyperactivity with increased futile cycles of carbohydrate metabolism in the LB Type 2 DM patients. These hepatic metabolic features are likely to be responsible for excess insulin utilization and extraction during first pass in the liver, leading to low peripheral circulating levels. Homocysteine levels, a non-lipid risk factor for atherosclerosis, are also low suggesting efficient metabolic status. Autoimmune destruction of beta-cells is not the cause of hypoinsulinemia as levels of islet cell and anti-glutamic acid decarboxylase (GAD) antibodies are similar to those in patients with classical Type 2 DM and much lower than those in Type 1 DM. The metabolic profile reveals normal high density lipoprotein (HDL) cholesterol levels with Type-IV hyperlipoproteinemia in glycemic uncontrolled states. Proteinuria found in uncontrolled metabolic states often reverses, suggesting endothelial cell dysfunction.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.