A Comparative Study of Antidiabetic Effect of Zinc,Chromium and Selenium Nanoparticles in Rats
Rasha Mustafa Hassan Amin;
Abstract
Diabetes mellitus (DM) is an overall medical problem that requires critical consideration; it may increase the susceptibility to many infections and other disorders.(T2DM) is known as a serious socio-economic problem and its prevalence increased worldwide. This type of diabetes is a complex and heterogeneous disorder is distinguished by a progressive decline in insulin action or defect in insulin signal transduction. It is strongly associated with obesity and insulin resistance as well as defects in pancreatic β-cell function and mass. These metabolic disorders impede the critical regulatory influence of insulin on glucose, lipid and protein metabolism, thus precipitating a disease characterized by impairments in these physiological processes.
However, it takes years to develop T2DM. Patients developing type 2 diabetes have often gone through a state of obesity associated with reduced insulin sensitivity along with an activated β-cell compensatory mechanism, such as excess basal insulin secretion and hyper-proinsulinemia, as a part of their metabolic profile. These pathological conditions occur early in the disease progression of T2DM, and before the β-cells severely fail in late stage (insulin-dependent) T2DM. STZ has been used alone or in combination with other chemicals or with dietary manipulations for induction of either type 1 or type 2diabetes. Fructose intake in excess can induce moderate obesity and have several deleterious metabolic effects, including hyper-triglyceridemia and hyperinsulinaemia.
Recent advances include the discovery of novel genes that are regulated by peroxisome proliferator activated receptor (PPAR-γ), which helps explain how activation of this adipocyte predominant transcription factor regulates glucose and lipid homeostasis. PPAR-γ agonists ameliorate hyperglycemia, by reversing lipotoxicity induced insulin resistance. The insulin receptor substrate-1 (IRS-1) gene has been proposed as having a role in the insulin-resistant disorders.Its gene product, the IRS-1 protein, is a cytoplasm molecule expressed in most insulin-sensitive tissues and has been demonstrated to play a pivotal role in modulating the cellular effects of insulin.
However, it takes years to develop T2DM. Patients developing type 2 diabetes have often gone through a state of obesity associated with reduced insulin sensitivity along with an activated β-cell compensatory mechanism, such as excess basal insulin secretion and hyper-proinsulinemia, as a part of their metabolic profile. These pathological conditions occur early in the disease progression of T2DM, and before the β-cells severely fail in late stage (insulin-dependent) T2DM. STZ has been used alone or in combination with other chemicals or with dietary manipulations for induction of either type 1 or type 2diabetes. Fructose intake in excess can induce moderate obesity and have several deleterious metabolic effects, including hyper-triglyceridemia and hyperinsulinaemia.
Recent advances include the discovery of novel genes that are regulated by peroxisome proliferator activated receptor (PPAR-γ), which helps explain how activation of this adipocyte predominant transcription factor regulates glucose and lipid homeostasis. PPAR-γ agonists ameliorate hyperglycemia, by reversing lipotoxicity induced insulin resistance. The insulin receptor substrate-1 (IRS-1) gene has been proposed as having a role in the insulin-resistant disorders.Its gene product, the IRS-1 protein, is a cytoplasm molecule expressed in most insulin-sensitive tissues and has been demonstrated to play a pivotal role in modulating the cellular effects of insulin.
Other data
| Title | A Comparative Study of Antidiabetic Effect of Zinc,Chromium and Selenium Nanoparticles in Rats | Other Titles | دراسة مقارنة للتأثير المضاد للسكري بواسطة مركبات الزنك والكروم والسيلينيوم النانونية في الجرذان. | Authors | Rasha Mustafa Hassan Amin | Issue Date | 2021 |
Attached Files
| File | Size | Format | |
|---|---|---|---|
| BB9173.pdf | 1.04 MB | Adobe PDF | View/Open |
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