Effect of 8 weeks HIIT exercise on myostatin, follistatin an follistatin gene expression ratios on myostatin in male rats with type 2 diabetes

Author(s):  
sepideh azhir ◽  
eidy alijani ◽  
mahsa mohsenzadeh
2021 ◽  
Vol 23 (1) ◽  
pp. 198
Author(s):  
Andrey A. Bakhtyukov ◽  
Kira V. Derkach ◽  
Viktor N. Sorokoumov ◽  
Anna M. Stepochkina ◽  
Irina V. Romanova ◽  
...  

In men with type 2 diabetes mellitus (T2DM), steroidogenesis and spermatogenesis are impaired. Metformin and the agonists of luteinizing hormone/human chorionic gonadotropin(hCG)-receptor (LH/hCG-R) (hCG, low-molecular-weight allosteric LH/hCG-R-agonists) can be used to restore them. The aim was to study effectiveness of separate and combined administration of metformin, hCG and 5-amino-N-tert-butyl-2-(methylsulfanyl)-4-(3-(nicotinamido)phenyl)thieno[2,3-d]pyrimidine-6-carboxamide (TP3) on steroidogenesis and spermatogenesis in male rats with T2DM. hCG (15 IU/rat/day) and TP3 (15 mg/kg/day) were injected in the last five days of five-week metformin treatment (120 mg/kg/day). Metformin improved testicular steroidogenesis and spermatogenesis and restored LH/hCG-R-expression. Compared to control, in T2DM, hCG stimulated steroidogenesis and StAR-gene expression less effectively and, after five-day administration, reduced LH/hCG-R-expression, while TP3 effects changed weaker. In co-administration of metformin and LH/hCG-R-agonists, on the first day, stimulating effects of LH/hCG-R-agonists on testosterone levels and hCG-stimulated expression of StAR- and CYP17A1-genes were increased, but on the 3–5th day, they disappeared. This was due to reduced LH/hCG-R-gene expression and increased aromatase-catalyzed estradiol production. With co-administration, LH/hCG-R-agonists did not contribute to improving spermatogenesis, induced by metformin. Thus, in T2DM, metformin and LH/hCG-R-agonists restore steroidogenesis and spermatogenesis, with metformin being more effective in restoring spermatogenesis, and their co-administration improves LH/hCG-R-agonist-stimulating testicular steroidogenesis in acute but not chronic administration.


2021 ◽  
Vol 27 (1) ◽  
pp. 82-97
Author(s):  
Samira Hassanpour Soleimani ◽  
◽  
Asiyeh Abbassi Daloii ◽  
Ahmed Abdi ◽  
Sheerin Zilaei Bori ◽  
...  

Aims: Type 2 diabetes is a rising problem and a significant risk factor for small and large vessel disease. The present study aims to investigate the effect of a 6-week aerobic exercise program on High-mobility Group Box 1 (HMGB1) gene expression in aortic tissue of diabetic rats. Methods & Materials: In this experimental study, 40 male rats aged 8 weeks were randomly selected. Once familiarized with the exercise protocol, they were divided into four groups of healthy-control (n=10), diabetic-control (n=10), healthy-exercise (n=10), and diabetic-exercise (n=10). Type 2 diabetes was first induced, and then the rats run on a treadmill for 6 weeks, 5 sessions per week. After 12-14 h of fasting and 72 h after the last session, aortic tissue sampling was performed for HMGB1 analysis by quantitative real-time polymerase chain reaction (q-RT PCR) technique. Data analysis was performed using 1-way ANOVA and Tukey post hoc test at the significant level of P<0.05. Findings: Induction of type 2 diabetes led to a significant increase in HMGB1 gene expression in rats (P=0.001), significantly reduced following aerobic exercise (P=0.003). Aerobic exercise also reduced the expression of the HMGB1 gene in healthy rats (P=0.000). Conclusion: Aerobic exercise may have a protective effect by reducing the HMGB1 gene expression in the aortic tissue of diabetic rats. It can be used as an effective non-pharmacological method to improve diabetes-induced inflammation and prevent vascular disorders.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 52-LB
Author(s):  
MAYSA SOUSA ◽  
ARITANIA SANTOS ◽  
MARIA ELIZABETH R. SILVA

Author(s):  
Zarish Noreen ◽  
Christopher A. Loffredo ◽  
Attya Bhatti ◽  
Jyothirmai J. Simhadri ◽  
Gail Nunlee-Bland ◽  
...  

The epidemic of type 2 diabetes mellitus (T2DM) is an important global health concern. Our earlier epidemiological investigation in Pakistan prompted us to conduct a molecular investigation to decipher the differential genetic pathways of this health condition in relation to non-diabetic controls. Our microarray studies of global gene expression were conducted on the Affymetrix platform using Human Genome U133 Plus 2.0 Array along with Ingenuity Pathway Analysis (IPA) to associate the affected genes with their canonical pathways. High-throughput qRT-PCR TaqMan Low Density Array (TLDA) was performed to validate the selected differentially expressed genes of our interest, viz., ARNT, LEPR, MYC, RRAD, CYP2D6, TP53, APOC1, APOC2, CYP1B1, SLC2A13, and SLC33A1 using a small population validation sample (n = 15 cases and their corresponding matched controls). Overall, our small pilot study revealed a discrete gene expression profile in cases compared to controls. The disease pathways included: Insulin Receptor Signaling, Type II Diabetes Mellitus Signaling, Apoptosis Signaling, Aryl Hydrocarbon Receptor Signaling, p53 Signaling, Mitochondrial Dysfunction, Chronic Myeloid Leukemia Signaling, Parkinson’s Signaling, Molecular Mechanism of Cancer, and Cell Cycle G1/S Checkpoint Regulation, GABA Receptor Signaling, Neuroinflammation Signaling Pathway, Dopamine Receptor Signaling, Sirtuin Signaling Pathway, Oxidative Phosphorylation, LXR/RXR Activation, and Mitochondrial Dysfunction, strongly consistent with the evidence from epidemiological studies. These gene fingerprints could lead to the development of biomarkers for the identification of subgroups at high risk for future disease well ahead of time, before the actual disease becomes visible.


2009 ◽  
Vol 41 (12) ◽  
pp. 899-904 ◽  
Author(s):  
A. I. Taylor ◽  
N. Frizzell ◽  
A. M. McKillop ◽  
P. R. Flatt ◽  
V. A. Gault

2005 ◽  
Vol 34 (2) ◽  
pp. 299-315 ◽  
Author(s):  
Young Ho Suh ◽  
Younyoung Kim ◽  
Jeong Hyun Bang ◽  
Kyoung Suk Choi ◽  
June Woo Lee ◽  
...  

Insulin resistance occurs early in the disease process, preceding the development of type 2 diabetes. Therefore, the identification of molecules that contribute to insulin resistance and leading up to type 2 diabetes is important to elucidate the molecular pathogenesis of the disease. To this end, we characterized gene expression profiles from insulin-sensitive tissues, including adipose tissue, skeletal muscle, and liver tissue of Zucker diabetic fatty (ZDF) rats, a well characterized type 2 diabetes animal model. Gene expression profiles from ZDF rats at 6 weeks (pre-diabetes), 12 weeks (diabetes), and 20 weeks (late-stage diabetes) were compared with age- and sex-matched Zucker lean control (ZLC) rats using 5000 cDNA chips. Differentially regulated genes demonstrating > 1.3-fold change at age were identified and categorized through hierarchical clustering analysis. Our results showed that while expression of lipolytic genes was elevated in adipose tissue of diabetic ZDF rats at 12 weeks of age, expression of lipogenic genes was decreased in liver but increased in skeletal muscle of 12 week old diabetic ZDF rats. These results suggest that impairment of hepatic lipogenesis accompanied with the reduced lipogenesis of adipose tissue may contribute to development of diabetes in ZDF rats by increasing lipogenesis in skeletal muscle. Moreover, expression of antioxidant defense genes was decreased in the liver of 12-week old diabetic ZDF rats as well as in the adipose tissue of ZDF rats both at 6 and 12 weeks of age. Cytochrome P450 (CYP) genes were also significantly reduced in 12 week old diabetic liver of ZDF rats. Genes involved in glucose utilization were downregulated in skeletal muscle of diabetic ZDF rats, and the hepatic gluconeogenic gene was upregulated in diabetic ZDF rats. Genes commonly expressed in all three tissue types were also observed. These profilings might provide better fundamental understanding of insulin resistance and development of type 2 diabetes.


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