Original Data

The Relationship between Dietary Habits, Blood Glucose and Insulin Levels among People without Cardiovascular Disease and Type 2 Diabetes; The ATTICA Study

Demosthenes B. Panagiotakos¹, Natalia Tzima¹, Christos Pitsavos², Christina Chrysohoou², Emilia Papakonstantinou¹, Antonis Zampelas¹, Christodoulos Stefanadis²

Abstract

BACKGROUND: Diet has long been associated with a risk of insulin resistance and poor glycemic control. We sought to investigate the association between food groups and indices of glycemic control in adults without type 2 diabetes and cardiovascular disease. METHODS: During 2001 - 2002 we randomly enrolled 1514 men (18-87 years old) and 1528 women (18-89 years old) without evidence of cardiovascular disease from the Attica area of Greece. Of them, 118 men and 92 women were excluded from the present analysis due to a history of diabetes mellitus (type 2). Fasting blood glucose and insulin levels were measured, while dietary habits were evaluated through a semi-quantitative food frequency questionnaire. RESULTS: Red meat consumption was positively associated with hyperglycemia (p = 0.04), hyperinsulinemia (p = 0.04), and HOMA levels (p = 0.03), even after adjusting for BMI and various other potential confounders. The intake of fruits, vegetables, legumes, yogurt and other dairy products was not associated with levels of glycemic control indices. CONCLUSIONS: A higher consumption of red meat and its products may aggravate hyperinsulinemia and insulin resistance in non-diabetic people.

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Effect of Losartan on the mRNA Expressions of MT3-MMP and TIMP-2 in Diabetic Kidneys

He-Lin Ding, Ming-Tong Xu, Ying Guo, Long Chen, Shao-Ling Zhang, Feng Li, Zu-Zhi Fu

Abstract

BACKGROUND and OBJECTIVES: The renin-angiotensin system plays a critical role in circulatory homoeostasis. Evidence has emerged that suggests a pathologic role for angiotensin II in patients with kidney disease. Losartan is an antagonist of angiotensin II and blocks the angiotensin II type-1 receptor. Thus it may reduce proteinuria and delay the progression of renal disease in diabetic nephropathy. We investigated the effects of losartan on the mRNA expressions of membrane-type3 matrix metalloproteinases (MT3-MMP) and the tissue inhibitor of metalloproteinase-2 (TIMP-2) in diabetic kidneys in order to evaluate degradation and remodeling of the extracellular matrix. METHODS: Male Wistar rats were divided into 3 groups. Group A was the control group containing healthy rats (n = 11), group B comprised diabetic rats without any therapy (n = 11), and group C consisted of diabetic rats treated with losartan (n = 9). 24-hr urine samples were collected in order to measure urinary albumin excretion (UAE). After a period of 18 weeks, the kidneys were extracted from all rats in order to measure the mRNA expressions of MT3-MMP, TIMP-2 and transforming growth factor-β1 (TGF-β1) by RT-PCR. We also examined the glomerular basement membrane thickening and the mesangial matrix (MM) density (MM area/mesangial area). RESULTS: The expression of renal MT3-MMP mRNA in group B (1.37 ± 0.96) was significantly higher than that in group A (0.75 ± 0.34, p < 0.05), but also significantly higher than in group C (0.75 ± 0.30, p < 0.05). Similarly, the mRNA expression of renal TIMP-2 in group B (0.73 ± 0.37) was significantly increased compared to that in group A (0.32 ± 0.19, p < 0.05), but also higher than in group C (0.34 ± 0.17, p < 0.05). In addition, subjects in group B showed abundant TGF-β1 mRNA expression and UAE compared to groups A and C, as well as significantly higher glomerular basement membrane thickening and MM density (all p < 0.05). CONCLUSIONS: We conclude that MT3-MMP and TIMP-2 production in the renal cortex of diabetic kidneys is increased. Losartan can prevent the development of diabetic nephropathy by decreasing MT3-MMP and TIMP2 production in diabetic kidneys.

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Shell-Less Chick Embryo Culture as an Alternative in vitro Model to Investigate Glucose-Induced Malformations in Mammalian Embryos

Savita Datar¹, Ramesh R. Bhonde²

Abstract

We have developed a simple shell-less chick embryo culture system to study glucose-induced malformations. This system involves the culturing of chick embryos from the second day to the fifth day of incubation, with associated yolk and thick and thin albumen outside the egg shell. The system allows the observation of embryonic development of chicks in a glass bowl. Developing embryos at 24 h, 48 h and 72 h incubation, corresponding to the Hamberger Hamilton (HH) stages from 7 to 21, were treated with two concentrations of glucose (50 mM and 100 mM) for 24 h. Glucose treatment resulted in a mortality rate of over 70% in younger embryos. Furthermore, a variety of malformations such as retarded growth, abnormal heart development, macrosomia, exencephaly, etc. were observed in older embryos, which were similar to those reported in mammalian embryos as a consequence of diabetic pregnancy. The glucose-induced malformations were found to be concentration- and stage-dependent, thus emphasizing the roles of the degree of hyperglycemia and the stage of embryonic development in diabetic growth anomalies. Here we demonstrate for the first time that the present system can be used (i) for experiments at early stages of chick embryo development and (ii) for assessing the effects of acute glucose toxicity similar to those reported for mammalian embryos in a hyperglycemic environment.

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