Diabetes type models

Knockout mice have been reported for several FATPs [1]. As insulin desensitization has been closely linked to excessive fatty acid uptake and intracellular diacylgly-cerol and TG accumulation, these animal models were particularly evaluated in the context of protection from diet-induced type 2 diabetes ( Type 2 Diabetes Mellitus (T2DM)). In addition, studies on human subjects have also established genetic links between polymorphisms in FATP genes and metabolic alterations [1]. 

Shinomiya, K., Fukunaga, M., Kiyomoto, H., Mizushige, K., Tsuji, T., Noma, T., Ohmori, K., Kohno, M., and Senda, S. 2002. A role of oxidative stress-generated eicosanoid in the progression of arteriosclerosis in type 2 diabetes mellitus model rats. Hypertens. Res. 25, 91-98. 

Treatment with either vanadium salts or organic complexes of vanadium have decreased plasma insulin levels and improved insulin sensitivity in animal models of both insulin resistance and type 2 diabetes. This work has recently been reviewed [13]. The Zucker Diabetic Fatty (ZDF) rat develops overt hyperglycemia in the presence of hyperinsulinemia followed by [3-cell depletion. This is a type 2 diabetic rat model developed from the Zucker Fatty (fa/fa) rat. In these animals, chronic treatment with vanadium reduced the elevated plasma glucose levels [152,153], The effect in the type 2 models of diabetes can take weeks to develop, whereas the effect in the type 1 models of diabetes are seen within 3 to 4 days. 

Studies using experimental diabetic animal models have indicated that xenobiotic-induced hepatotoxicity is modulated in diabetes. Hepatotoxicity of several structurally and mechanistically diverse chemicals, such as chloroform, thioacetamide, menadione, nitro-soamines, bromobenzene, and CCI4, is significantly increased in type 1 diabetic rats. It was reported that thioacetamide-induced hepatotoxicity was potentiated in alloxan- or streptozotocin-diabetic rats. Recent studies have confirmed the potentiation of thioacetamide hepatotoxicity in streptozotocin-diabetic rats. Several studies have shown that hepatotoxicity of CCI4 is potentiated in alloxan- or streptozotocin-induced type 1 diabetic rats. 

Almost all of the work examining modulation of xenobiotic-induced hepatotoxicity in diabetes has been done using type 1 diabetic models. Recently, a study reported a novel high-fat diet-induced type 2 diabetic rat model and tested the susceptibility of these diabetic rats to several classical hepatotoxicants. On treatment with nonlethal or sublethal doses of allyl alcohol, CCI4, or thioacetamide, it was found that hepatotoxicity of all these toxicants is significantly increased in the type 2 diabetic rats. 

Although antibodies to bovine serum albumin have been reported m patients with newly diagnosed type 1 diabetes, this model is contentious, and conflicting data exist. 

Finally, one intriguing application of these plants is that of combating hypoglycemia. The freeze-dried juice of Cucurbita ficifolia fruits, for example, has been successfully used in the treatment of diabetes type 2 in Mexico. The hypoglycemic effect was demonstrated by estimating blood glucose levels in different experimental models on healthy mice, alloxan-diabetic mice, and alloxan-diabetic rats [30]. 

Signaling pathways are the target of a combination of Drosophila genetics to identify the genetic basis of diabetes type II and tmnors, followed by validation of identified taigets in a mouse model. 

The antidiabetic effects of chitosan and its derivatives were reported in diabetic animal models, type 1 and type 2. A number of studies have been reported in the literature. 

Chitosan and its derivative exhibited the great antihyperglycemic, antihyperlipidemic, and anti-hypocholesterolemic activities in type 1 and type 2 diabetic animal models. Moreover, chitin, chitosan, and their derivatives exhibited cholesterol-lowering activity in animal and clinical studies. Therefore, chitin, chitosan, and their derivatives can be promising candidates as potential material for protecting diabetes mellitus and lowering the cholesterol absorption. 

NOD mouse Diabetes type I model for chronic Makino et al. (1980) and... 

Inhibition of vascular smooth muscle cell (VSMC) prolifoation with consequent reduction of thickening of the vascular wall (intima-media thickness (IMT) Prevention of altered vascular blood flow, extracellular matrix deposition, basement membrane thickening, and neovascularization during diabetes and insulin resistance Reduction of collagen accumulation in type 11 diabetic rat model... 

Kolberg JA, Jorgensen T, Gerwien RW, Hamren S, McKenna MP, Moler E, Rowe MW, Urdea MS, Xu XM, Hansen T, Pedersen O, Borch-Johnsen K. Tethys Bioscience, Emeryville, California, USA. jkolberg tethysbio.com Development of a type 2 diabetes risk model from a panel of serum biomarkers from the Inter99 cohort. Diabetes Care. 2009 Jul 32(7) 1207-12. 

In recent researches, stem cells have brought to new hope. Bone marrow with two major stem cells (hematopoietic and mesenchymal stem cells), the adult bone-marrow derived stem cells can regenerate the fl cell in diabetes animal models. These results lead to a new approach in diabetes treatment, especially type 1 diabetes. 

In the two grafted methods, intravenous injection had better result. In the three tested cell types (bone marrow cells, mesenchymal stem cells, stem cell derived insulin secreting cells), the insulin producing cell derived from mesenchymal stem cell had the best effect on recovering the insulin and blood sugar level in diabetes mouse model. 

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