scholarly journals Animal Models as Tools for Translational Research: Focus on Atherosclerosis, Metabolic Syndrome and Type-II Diabetes Mellitus

10.5772/47769 ◽  
2012 ◽  
Author(s):  
Isaac Karimi
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Animal Models ◽  
Translational Research ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Research Focus

scholarly journals A case study wistar rats by implementing Metformin on Clozapine

2018 ◽  
Vol 8 (1) ◽  
pp. 5-9
Author(s):  
Vinaya B ◽  
Akila CR ◽  
Dinesh Babu J ◽  
Sravan Kumar P
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Type Ii Diabetes ◽  
Wistar Rats ◽  
Fasting Blood Glucose ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Metabolic Derangement ◽  
Group 2 ◽  
The Impact

The medical studies in beyond decade has reported that maximum 2nd-era antipsychotics (SGAs) can reason severe metabolic derangement, which significantly upsurges the danger for type II diabetes mellitus. Numerous retrospective studies have proven multiplied in serum triglyceride in sufferers handled with Clozapine. SGAs triggered metabolic syndrome is characterized via hypertension, weight gain, hyperglycaemia, hyperlipidaemia, glucose intolerance and insulin resistance. Metformin is presently used to extravagance metabolic syndrome and type II diabetes mellitus. It is consequently essential to decide whether Metformin is effective in discussing Clozapine-brought on metabolic derangement like dyslipidaemia. To appraise the impact of Metformin in minimizing Clozapine caused metabolic irrationality like dyslipidaemia. Methodology: Wistar rats weighing a hundred and eighty-240g both intercourse had been divided into three corporations of 6 rats every. Group 1 attended as manipulate, Group 2 Preserved with Clozapine 25mg/kg frame weight and Group 3 Treated with Clozapine 25mg + Metformin 100mg/kg body weight for 30 days P.O. Group 2 and group three were preserved for 30 days. Lipid profile of institution 2 rats handled with Clozapine showed dyslipidaemia (TG 103.3±1.7mg/dl, Tc 113.7±1.6mg/dl). Whereas organization 3 rats treated with Clozapine 25mg + Metformin confirmed ordinary lipid levels (TG ninety four.7±1.7mg/dl, TC 102.Eight±0.Eight mg/dl) similar to institution 1(TG ninety three.0±2.6mg/dl, TC 103.7±1.5mg/dl). This study focuses a non-substantial increase in fasting blood glucose in SD rodents managed with clozapine that was in part checked by utilizing simultaneous organization of metformin. Rodents controlled clozapine affirmed the anticipated abatement in the statement of GLUT2, anyway simultaneous administration of metformin and clozapine for 30 days didn't show the anticipated standardization of the articulation degrees of GLUT2. This look at investigating the use of Metformin to forestall metabolic unsettling like dyslipidaemias in patients of schizophrenia managed with Clozapine.

scholarly journals ROLE OF METFORMIN ON CLOZAPINE INDUCED DYSLIPIDAEMIA IN WISTAR RATS

2018 ◽  
pp. 1-5
Author(s):  
Syed Shoib Md Hussaini ◽  
Akram A Naikwadi ◽  
Narsapur VU
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Type Ii Diabetes ◽  
Wistar Rats ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Metabolic Derangement ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Background: The clinical research in past decade has reported that most second-generation antipsychotics (SGAs) can cause serious metabolic derangement, which substantially increases the risk for type II diabetes mellitus. Several retrospective studies have shown increased in serum triglyceride in patients treated with Clozapine. SGAs induced metabolic syndrome is characterized by weight gain, hyperglycaemia, hypertension, hyperlipidaemia, glucose intolerance and insulin resistance. Metformin is currently used to treat metabolic syndrome and type II diabetes mellitus. It is therefore important to determine whether Metformin is efficacious in treating Clozapine-induced metabolic derangement like dyslipidaemia. Objectives: To evaluate the effect of Metformin in minimizing Clozapine induced metabolic derangement like dyslipidaemia. Methodology: Wistar rats weighing 180-240g either sex were divided into 3 groups of 6 rats each. Group 1 served as control, Group 2 Treated with Clozapine 25mg/kg body weight and Group 3 Treated with Clozapine 25mg + Metformin 100mg/kg body weight for 28 days P.O. Group 2 and group 3 were treated for 28 days. Biochemical investigations: Retro-orbital blood was collected for Lipid profile. Result: Lipid profile of group 2 rats treated with Clozapine showed dyslipidaemia (TG 103.3 ±1.7mg/dl, Tc 113.7 ±1.6mg/dl). Whereas group 3 rats treated with Clozapine 25mg + Metformin showed normal lipid levels (TG 94.7±1.7mg/dl, TC 102.8 ±0.8 mg/dl) comparable to group 1(TG 93.0 ±2.6mg/dl, TC 103.7 ±1.5mg/dl). Conclusion: This study exploring the use of Metformin to prevent metabolic derangement like dyslipidaemias in patients of schizophrenia treated with Clozapine. KEYWORDS: Clozapine; Metformin; Dyslipidaemia.

STUDIES ON APOLIPOPROTEINS (APO A1 & APO B) AND LIPOPROTEIN (A) ALONG WITH LIPID PROFILE IN THE PATIENTS OF TYPE II DIABETES MELLITUS AND METABOLIC SYNDROME

2020 ◽  
Vol 4 (2) ◽  
Author(s):  
Arpita Rohit ◽  
N. Haridas
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Lipid Profile ◽  
Apolipoprotein B ◽  
Type Ii Diabetes ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Apo B ◽  
Lipoprotein A ◽  
The Metabolic Syndrome

Patients with Type II diabetes mellitus or the metabolic syndrome have unique dyslipidemia characterized by hypertriglyceridemia; elevated blood levels of apolipoprotein B; small, dense low-density lipoprotein (LDL) cholesterol; and low levels of high-density lipoprotein (HDL) cholesterol. Treatment of dyslipidemia associated with these disorders should focus on correcting the abnormal lipoprotein levels as well as LDL and HDL heterogeneity. Statins and fibrates are useful for treating elevated LDL in patients with and without diabetes or the metabolic syndrome. There are few researches on Apolipoprotein A and Apolipoprotein B, Lipoprotein (a) in India, in comparison to foreign countries. So this study is aimed to evaluate Apo lipoproteins (Apo A1 & Apo B) and Lipoprotein (a) levels along with Lipid profile in Type II Diabetes Mellitus and in patients with Metabolic Syndrome which can be correlated with the risk of cardiovascular disease. Conclusion: Apo lipoprotein A1, Apolipoprotein B and Lipoprotein (a) can be important marker for the risk developing of heart disease. Statistical relationships between LDL and HDL and their respective Apo lipoproteins, Apo B and Apo A-1, in diabetic and metabolic syndrome can be established. Keywords:  Lipid profile, Type II Diabetes Mellitus, Apo lipoproteins (Apo A & Apo B), Lipoprotein (a) and Metabolic Syndrome.

scholarly journals Heightened efficacy of nitric oxide-based therapies in type II diabetes mellitus and metabolic syndrome

2008 ◽  
Vol 295 (6) ◽  
pp. H2388-H2398 ◽  
Author(s):  
Sadaf S. Ahanchi ◽  
Vinit N. Varu ◽  
Nick D. Tsihlis ◽  
Janet Martinez ◽  
Charles G. Pearce ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Diabetes Mellitus ◽  
Cell Cycle ◽  
Metabolic Syndrome ◽  
Type Ii Diabetes ◽  
Neointimal Hyperplasia ◽  
Type Ii Diabetes Mellitus ◽  
Type Ii ◽  
Rodent Models ◽  
Cycle Arrest

Type II diabetes mellitus (DM) and metabolic syndrome are associated with accelerated restenosis following vascular interventions due to neointimal hyperplasia. The efficacy of nitric oxide (NO)-based therapies is unknown in these environments. Therefore, the aim of this study is to examine the efficacy of NO in preventing neointimal hyperplasia in animal models of type II DM and metabolic syndrome and examine possible mechanisms for differences in outcomes. Aortic vascular smooth muscle cells (VSMC) were harvested from rodent models of type II DM (Zucker diabetic fatty), metabolic syndrome (obese Zucker), and their genetic control (lean Zucker). Interestingly, NO inhibited proliferation and induced G0/G1 cell cycle arrest to the greatest extent in VSMC from rodent models of metabolic syndrome and type II DM compared with controls. This heightened efficacy was associated with increased expression of cyclin-dependent kinase inhibitor p21, but not p27. Using the rat carotid artery injury model to assess the efficacy of NO in vivo, we found that the NO donor PROLI/NO inhibited neointimal hyperplasia to the greatest extent in type II DM rodents, followed by metabolic syndrome, then controls. Increased neointimal hyperplasia correlated with increased reactive oxygen species (ROS) production, as demonstrated by dihydroethidium staining, and NO inhibited this increase most in metabolic syndrome and DM. In conclusion, NO was surprisingly a more effective inhibitor of neointimal hyperplasia following arterial injury in type II DM and metabolic syndrome vs. control. This heightened efficacy may be secondary to greater inhibition of VSMC proliferation through cell cycle arrest and regulation of ROS expression, in addition to other possible unidentified mechanisms that deserve further exploration.

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