scholarly journals Hyperinsulinemia Induced Altered Insulin Signaling Pathway in Muscle of High Fat- and Carbohydrate-Fed Rats: Effect of Exercise

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Anu Joseph ◽  
S. Parvathy ◽  
Koyikkal Karthikeya Varma

Insulin resistance is a state of impaired responsiveness to insulin action. This condition not only results in deficient glucose uptake but increases the risk for cardiovascular diseases (CVD), stroke, and obesity. The present work investigates the molecular mechanisms of high carbohydrate and fat diet in inducing prediabetic hyperinsulinemia and effect of exercise on InsR signaling events, muscular AChE, and lactate dehydrogenase activity. Adult male Wistar rats were divided into the control (C) diet group, high-carbohydrate diet (HCD) group, high-fat diet (HFD) group, and HCD and HFD groups with exercise (HCD Ex and HFD Ex, respectively). Acetyl choline esterase activity, lactate dehydrogenase activity, total lactate levels, IRS1 phosphorylations, and Glut4 expression patterns were studied in the muscle tissue among these groups. High carbohydrate and fat feeding led to hyperinsulinemic status with reduced acetylcholine esterase (AChE) activity and impaired phosphorylation of IRS1 along with increased lactate concentrations in the muscle. Exercise significantly upregulated phosphoinositide 3 kinase (PI3K) docking site phosphorylation and downregulated the negative IRS1 phosphorylations thereby increasing the glucose transporter (GLUT) expressions and reducing the lactate accumulation. Also, the levels of second messengers like IP3 and cAMP were increased with exercise. Increased second messenger levels induce calcium release thereby activating the downstream pathway promoting the translocation of GLUT4 to the plasma membrane. Our results showed that the metabolic and signaling pathway dysregulations seen during diet-induced hyperinsulinemia, a metabolic condition seen during the early stages in the development of prediabetes, were improved with vigorous physical exercise. Thus, exercise can be considered as an excellent management approach over drug therapy for diabetes and its complications.

1987 ◽  
Vol 6 (4) ◽  
pp. 555-560 ◽  
Author(s):  
David Sempol ◽  
Edurado Osinaga ◽  
Seymour Zigman ◽  
Israel Korc ◽  
Beatriz Korc ◽  
...  

2006 ◽  
Vol 31 (4) ◽  
pp. 541-548 ◽  
Author(s):  
Laura O. Saad ◽  
Sandra R. Mirandola ◽  
Evelise N. Maciel ◽  
Roger F. Castilho

2004 ◽  
Vol 17 (3) ◽  
pp. 204-206 ◽  
Author(s):  
H. Schmidt ◽  
M. Otto ◽  
P. Niedmann ◽  
L. Cepek ◽  
A. Schröter ◽  
...  

2019 ◽  
Author(s):  
Zhixiong Zhou ◽  
Xiaolin Dong ◽  
Chuanren Li

AbstractThe Chinese citrus fruit fly,Bactrocera minax, is a devastating citrus pest in China, Bhutan and India. It will enter obligatory pupal diapause in each generation at specific stage, while little is known about the course and the molecular mechanisms of diapause induction. To gain insight into possible mechanisms of obligatory pupal diapause induction, high-throughput RNA-seq data were generated from second-instar larvae (2L), third-instar larvae (3L) and pupal (P, one week after pupating). A total of 116,402 unigenes were assembled and researched against public databases, and 54,781 unigenes matched to proteins in the NCBI database using the BLAST search. Three pairwise comparisons were performed, and significantly differentially regulated transcripts were identified. Several differentially expressed genes (DEGs) expression patterns revealed that those highly or lowly expressed genes in pupal stage were predicted to be involved in diapause induction. Moreover, GO function and KEGG pathway analysis were performed on all DEGs and showed that 20-hydroxyecdysone (20E) biosynthesis, insulin signaling pathway, FoxO signaling pathway, cell cycle and metabolism pathway may be related to the obligatory diapause of the Chinese citrus fruit fly. This study provides valuable information about the Chinese citrus fruit fly transcriptome for future gene function research, and contributes to the in-depth elucidation of the molecular regulation mechanism of insect obligatory diapause induction.


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