Animal Models of Nutritional Induction of Type 2 Diabetes Mellitus

Abstract

SUMMARY:Type 2 diabetes mellitus (DM2) is the most common chronic metabolic disease, affecting approximately 6% of the adult population in the Western world. This condition is a major cause of cardiovascular disease, blindness, renal failure, and amputations, with increasing prevalence worldwide. The influence of obesity on type 2 diabetes risk is determined by the degree of obesity and by body fat localization, with insulin resistance (IR) being the main link between these metabolic diseases. Experimental studies have shown that dietary factors, and particularly lipids, are strongly positively associated with body mass (BM) gain; IR; and, consequently, type 2 diabetes. Similarly, excessive consumption of energy-dense carbohydrate-rich foods can trigger the onset of type 2 diabetes. Additionally, maternal dietary inadequacies at conception and/or during the gestational period have been proposed to lead to developmental programming of excessive BM gain and metabolic disturbances in offspring, such as abnormal glucose homeostasis, reduced wholebody insulin sensitivity, impaired beta-cell insulin secretion and changes in the structure of the pancreas. Metabolic disruption is strongly associated with deleterious effects on beta-cell development and function. However, alterations in the amount and quality of dietary fat can modify glucose metabolism and insulin sensitivity. In this way, certain oils have gained attention in experimental research for their beneficial effects. Olive oil, a source of monounsaturated fatty acids (MUFAs), got attention in the past for its capacity to prevent cardiovascular diseases. Nevertheless, it is currently known that this oil also improves insulin sensitivity and glycemic control. Canola oil, flaxseed oil and especially fish oil (rich in n-3 polyunsaturated fatty acids) were first described as effective dietary nutrients against hypertriglyceridemia but now are known to have positive effects on glucose metabolism as well.

RETRACTED ARTICLE: Troxerutin reverses fibrotic changes in the myocardium of high-fat high-fructose diet-fed mice

“…In humans and rodents, intake of a diet rich in fructose and fat produces insulin resistance (and/or hyperglycemia) and metabolic changes in tissues [2,3]. A number of structural and functional changes in the myocardium such as cardiac hypertrophy, cardiac fibrosis, and ventricular contractile dysfunction and cardiovascular remodeling are reported in high-fat high-fructose diet-fed rats [4,5].…”

Diet-Induced Rodent Models of Diabetic Peripheral Neuropathy, Retinopathy and Nephropathy

“…It is generally believed that T2DM is driven by a complex interplay of genetic factors and unhealthy lifestyle habits comprising an energy-dense "westernized" diet [10][11][12][13][14]. Hence, diet-induced rodent models of T2DM, whether alone or combined with genetic/chemical stressors, are paramount to more closely replicate human microvascular complications [15,16]. The most commonly used diets for T2DM animal research are high-fat diets (HFD), high-sugar diets (HSD), and Western diets combining both high-fat and high-sugar components (HFSD) [17].…”

Evaluation of Anti-Obesity Activity of an Herbal Formulation (F2) in DIO Mice Model and Validation of UPLC-DAD Method for Quality Control

“…This condition has been termed as compensatory hyperinsulinemia [45]. The previous literature has also revealed that dietary high-fat leads to promote insulin resistance and hyperinsulinemia before the development of type 2 diabetes in rodents [48][49][50]. High-fat diet-induced hyperinsulinemia or insulin resistance may occur due to a decrease in the glucose transporter, insulin receptors, and glucose metabolism [10,28].…”