Insulin Secretion and Sensitivity in Newly Diagnosed NIDDM Caucasians in the UK

Abstract

Beta-cell secretion and insulin sensitivity was studied in healthy subjects and newly diagnosed Caucasian (Welsh) NIDDM patients. A standardized meal tolerance test (MTT) and frequent sampled intravenous glucose tolerance tests (FSIVGTT) were employed and the patients stratified according to fasting plasma glucose (FPG). A deficient early (first hour) post-prandial (MTT) insulin secretion was demonstrated in all NIDDM patients, deteriorating with increasing fasting hyperglycaemia. For the patient group fasting and post-prandial hyperproinsulinaemia was evident with diminishing post-prandial excursions as fasting hyperglycaemia increased. The early phase (0-10 min) insulin secretion to intravenous glucose (300 mg kg-1 ) was severely impaired in NIDDM patients. A shortlived paradoxical fall in plasma insulin concentrations was observed in those with FPG >9 mmoll-1 • Insulin sensitivity utilizing the insulin modified FSIVGTT demonstrated that all NIDDM patients had marked insulin insensitivity. Characteristic of the newly diagnosed previously untreated Caucasian NIDDM is a dysfunctional beta cell, resulting in a deficit in insulin secretion with relative hyperproinsulinaemia. The quantitative and qualitative secretory status of the beta cell decreases with increasing fasting hyperglycaemia. Insulin sensitivity is markedly reduced when FPG exceeds 7.0 mmol J-1 with little or no further discernible fall with deteriorating glycaemic control.

Insulin Hyposecretion in Nondiabetic, Tacrolimus-Treated Renal Transplant Recipients More Than 6 months Posttransplantation

“…After an overnight fast, the subjects were examined with a meal tolerance test (MTT) (21) and a frequently sampled, insulin-modified intravenous glucose tolerance test (21,22). Both these tests were undertaken strictly in accordance with standard operating protocols derived from the Diabetes Research Unit.…”

Anti-dyslipidemic and antioxidant activities of different fractions of Pongamia pinnata (lin.) fruits

“…We have employed HFD-induced diabetes-dyslipidemia in hamster, which is a very suitable model for screening of drugs for the regulation of lipid and carbohydrate metabolism (Trinder 1969;Bhatia et al 2003). Feeding with the active fraction of P. pinnata resulted in a lowering of plasma lipid and glucose, suggesting that this property of test sample is mediated through peroxisomes proliferate-activated receptors -a subtype (PPAR-a) in diversified manner by catabolizing Tg, upregulating lipoprotein lipases to rid off dietary load, and improve the HDL levels for the maintenance of lipid-glucose homeostasis in hamster model (Wako pure chemicals ltd., NAFAC 1996;Ownes 1996). To asses the antioxidant activity of P. pinnata fractions in rat liver microsomes for oxidation as an in vitro model of nonenzymic stimulation of lipid peroxidation mediated by the action of OH -radicals (Zilversmit et al 1950) in the present study ethanolic fractions of P. pinnata fruits inhibited microsomal lipids and also suppressed the generation of OHradicals in the above tests.…”

Control of Postprandial Glucose Levels with Insulin in Type 2 Diabetes

“…In T2DM, fi rst-phase insulin and incretin responses are severely diminished or absent, resulting in persistently elevated PPG. 34,38 Lack of insulin activity is often further compounded by severely reduced insulin sensitivity, so that the insulin that is present cannot adequately suppress hepatic glucose production or increase glucose uptake. 1,39 Furthermore, patients with T2DM also have diminished (and/or are resistant to the effects of) amylin and GLP-1; hence, postprandial glucagon secretion is not fully suppressed and glucose continues to be released from the liver, further elevating already increased PPG levels.…”