Original Data

Differential Postprandial Lipoprotein Responses in Type 2 Diabetic Men with and without Clinical Evidence of a Former Myocardial Infarction

Marius Carstensen¹, Claus Thomsen¹, Ole Gotzsche², Jens Juul Holst³, Jürgen Schrezenmeir⁴, Kjeld Hermansen¹

Abstract

Postprandial lipemia plays an important role in the development of coronary heart disease through an elevation of triglyceride-rich lipoproteins. In type 2 diabetic male subjects, our aim was to compare postprandial lipemia in a high-risk population with former myocardial infarction (MI) with that of a lower risk population free of clinically detectable heart disease. 32 male type 2 diabetic subjects were included in the study. We matched 17 cases with a verified history of MI with 15 controls according to age, BMI, HbA1c, diabetes duration, smoking, and treatment of diabetes. Ongoing metformin, insulin, or lipid lowering pharmacological treatment were exclusion criteria. After a maximal exercise tolerance test and echocardiography, the subjects underwent a hyperinsulinemic, euglycemic clamp and a vitamin A fat loading test. Plasma triglyceride levels in the case group were significantly higher after 360 minutes (4.6 ± 3.1 vs. 2.8 ± 1.8 mmol/l, p = 0.04) and 480 minutes (3.6 ± 2.2 vs. 2.4 ± 2.4 mmol/l, p = 0.03), as was the incremental Area Under the Curve (iAUC) for the whole period (560 ± 452 vs. 297 ± 214 mmolx480min./l; p = 0.048). In addition, the retinyl palmitate responses in the chylomicron-fraction from the case group were significantly higher (iAUC 311,502 ± 194,933 vs. 187,004 ± 102,928 ngx480min./ml; p = 0.035). Type 2 diabetic males with prior MI had higher postprandial triglyceride-rich lipoprotein responses than those without MI, indicating that high responses may be a marker for a high-risk population.

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Existence of Islet Regenerating Factors within the Pancreas

Meghana Kanitkar, Ramesh Bhonde

Abstract

Reduction in the functional mass of β-cells is a common denominator in most forms of diabetes. Since the replicative potential of β-cells is limited, the search for factors that trigger islet neogenesis becomes imperative. Here we tested the hypothesis that regenerating factors for the pancreas are either secreted by or present within the pancreatic milieu itself. For this purpose, we intraperitoneally injected pancreatic cell culture supernatant (PCCS), from normal pancreas, into streptozotocin(STZ)-induced diabetic mice for 15 consecutive days. The PCCS-treated mice showed sustained reversal in 77.77% of experimental diabetic mice as evidenced by restoration of normoglycemia, increase in serum insulin levels and occurrence of neo islets in histopathological studies during a two month follow up, as opposed to the control diabetic mice which remained hyperglycemic throughout. In order to examine the potential of PCCS to bring about the regeneration of islets, we treated intra-islet precursor cells with PCCS in vitro, which led to the neogenesis of islets as evidenced by dithiozone and insulin immunostaining. These findings substantiate our hypothesis and make the search for regenerative factors converge towards the pancreas and its immediate surroundings. Such regenerative approaches, in combination with other therapeutic strategies to promote islet neogenesis may, in future, provide a cure and/or better means for the control and management of diabetes.

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