Effects of high-fat diet on insulin receptor function in rat hippocampus and the level of neuronal corticosterone

Life Sciences ◽  
2011 ◽  
Vol 88 (13-14) ◽  
pp. 619-627 ◽  
Author(s):  
Wasana Pratchayasakul ◽  
Sasiwan Kerdphoo ◽  
Petnoi Petsophonsakul ◽  
Anchalee Pongchaidecha ◽  
Nipon Chattipakorn ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
High Fat Diet ◽  
Rat Hippocampus ◽  
Receptor Function ◽  
High Fat

scholarly journals Hyperinsulinemia Induces Insulin Receptor Dysfunction in Brain Microvascular Endothelial Cells

2021 ◽  
Author(s):  
Luke S. Watson ◽  
Brynna Wilken-Resman ◽  
Alexus Williams ◽  
Guadalupe Sanchez ◽  
Taylor Lowry McLeod ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Insulin Receptor ◽  
High Fat Diet ◽  
Insulin Receptors ◽  
Receptor Internalization ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Receptor Function ◽  
High Fat ◽  
Microvascular Endothelial

Insulin receptors are internalized by endothelial cells; however, the impact of hyperinsulinemia on this process is not known. Thus, the aim of this study is to determine the role of hyperinsulinemia on insulin receptor function and internalization, as well as the potential impact of protein tyrosine phosphatase 1B (PTP1B). To this end, hippocampal microvessels were isolated from male C57Bl/6J mice on either a control or high-fat diet and assessed for insulin receptor signaling. Cell surface insulin receptors in brain microvascular endothelial cells were labelled with biotin to assess the role hyperinsulinemia plays on receptor internalization in response to stimulation, with and without Claramine treatment, a potent PTP1B antagonist. Our results indicated that insulin receptor levels increased in tandem with insulin receptor dysfunction in the high-fat diet mouse hippocampal microvessels. Hyperinsulinemic cell-receptors demonstrate a shift in splice variation towards decreased IR-A/IR-B ratios and demonstrate a higher membrane-localized proportion. This corresponded with decreased autophosphorylation at sites critical for receptor internalization and signaling, however, Claramine restored signaling and receptor internalization in hyperinsulinemic cells. In conclusion, hyperinsulinemia negatively impacts brain microvascular endothelial cell insulin receptor function and internalization, likely through both alternative splicing and increased negative feedback from PTP1B.

scholarly journals Proximal tubular epithelial insulin receptor mediates high fat diet-induced kidney injury

JCI Insight ◽  
2021 ◽  
Author(s):  
Hak Joo Lee ◽  
Meenalakshmi M. Mariappan ◽  
Luke Norton ◽  
Terry Bakewell ◽  
Denis Feliers ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
High Fat Diet ◽  
Kidney Injury ◽  
High Fat ◽  
Proximal Tubular

Vitamin A status affects weight gain and hepatic glucose metabolism in rats fed a high-fat diet

2019 ◽  
Vol 97 (5) ◽  
pp. 545-553 ◽  
Author(s):  
Heqian Kuang ◽  
Cheng-hsin Wei ◽  
Tiannan Wang ◽  
Jennifer Eastep ◽  
Yang Li ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Vitamin A ◽  
Insulin Receptor ◽  
High Fat Diet ◽  
Glycogen Synthase ◽  
Mitogen Activated Protein Kinase ◽  
High Fat ◽  
Expression Levels ◽  
Hepatic Expression ◽  
Hepatic Glucose

Whether vitamin A (VA) has a role in the development of metabolic abnormalities associated with intake of a high-fat diet (HFD) is unclear. Sprague–Dawley rats after weaning were fed an isocaloric VA sufficient HFD (VAS-HFD) or a VA deficient HFD (VAD-HFD) for 8 weeks. Body mass, food intake, liver and adipose tissue mass, and the hepatic expression levels of key proteins for metabolism were determined. VAD-HFD rats had lower body, liver, and epididymal fat mass than VAS-HFD rats. VAD-HFD rats had lower hepatic protein expression levels of cytochrome P450 26A1, glucokinase, and phosphoenolpyruvate carboxykinase than VAS-HFD rats. VAD-HFD rats had higher protein levels of glycogen synthase kinase (GSK)-3α and lower levels of GSK-3β, but not glycogen synthase, than VAS-HFD rats. VAD-HFD rats had higher hepatic levels of insulin receptor substrate-1 (IRS-1), insulin receptor β-subunit, mitogen-activated protein kinase proteins, and peroxisome proliferator-activated receptor-gamma coactivator 1α mRNA, and lower level of IRS-2 protein than VAS-HFD rats. These results indicate that in a HFD setting, VA deficiency attenuated HFD-induced obesity, and VA status altered the expression levels of proteins required for glucose metabolism and insulin signaling. We conclude that VA status contributes to the regulation of hepatic glucose and lipid metabolism in a HFD setting, and may regulate hepatic carbohydrate metabolism.

Effect of High-Fat Diet on Gene Expression of GLUT4 and Insulin Receptor in Soleus Muscle

1994 ◽  
Vol 202 (1) ◽  
pp. 519-526 ◽  
Author(s):  
Y.B. Kim ◽  
T. Tomohiro ◽  
S. Iwashita ◽  
K. Tokuyama ◽  
M. Suzuki
Keyword(s):  
Gene Expression ◽  
Insulin Receptor ◽  
Soleus Muscle ◽  
High Fat Diet ◽  
High Fat

scholarly journals Pharmacological Administration of the Isoflavone Daidzein Enhances Cell Proliferation and Reduces High Fat Diet-Induced Apoptosis and Gliosis in the Rat Hippocampus

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64750 ◽  
Author(s):  
Patricia Rivera ◽  
Margarita Pérez-Martín ◽  
Francisco J. Pavón ◽  
Antonia Serrano ◽  
Ana Crespillo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
High Fat Diet ◽  
Rat Hippocampus ◽  
High Fat ◽  
Induced Apoptosis

scholarly journals Programming With Varying Dietary Fat Content Alters Cardiac Insulin Receptor, Glut4 and FoxO1 Immunoreactivity in Neonatal Rats, Whereas High Fat Programming Alters Cebpa Gene Expression in Neonatal Female Rats

2022 ◽  
Vol 12 ◽  
Author(s):  
Annelene Govindsamy ◽  
Samira Ghoor ◽  
Marlon E. Cerf
Keyword(s):  
Gene Expression ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Female Offspring ◽  
Fat Content ◽  
Neonatal Rats ◽  
Cardiac Physiology ◽  
High Fat

Fetal programming refers to an intrauterine stimulus or insult that shapes growth, development and health outcomes. Dependent on the quality and quantity, dietary fats can be beneficial or detrimental for the growth of the fetus and can alter insulin signaling by regulating the expression of key factors. The effects of varying dietary fat content on the expression profiles of factors in the neonatal female and male rat heart were investigated and analyzed in control (10% fat), 20F (20% fat), 30F (30% fat) and 40F (40% fat which was a high fat diet used to induce high fat programming) neonatal rats. The whole neonatal heart was immunostained for insulin receptor, glucose transporter 4 (Glut4) and forkhead box protein 1 (FoxO1), followed by image analysis. The expression of 84 genes, commonly associated with the insulin signaling pathway, were then examined in 40F female and 40F male offspring. Maintenance on diets, varying in fat content during fetal life, altered the expression of cardiac factors, with changes induced from 20% fat in female neonates, but from 30% fat in male neonates. Further, CCAAT/enhancer-binding protein alpha (Cebpa) was upregulated in 40F female neonates. There was, however, differential expression of several insulin signaling genes in 40F (high fat programmed) offspring, with some tending to significance but most differences were in fold changes (≥1.5 fold). The increased immunoreactivity for insulin receptor, Glut4 and FoxO1 in 20F female and 30F male neonatal rats may reflect a compensatory response to programming to maintain cardiac physiology. Cebpa was upregulated in female offspring maintained on a high fat diet, with fold increases in other insulin signaling genes viz. Aebp1, Cfd (adipsin), Adra1d, Prkcg, Igfbp, Retn (resistin) and Ucp1. In female offspring maintained on a high fat diet, increased Cebpa gene expression (concomitant with fold increases in other insulin signaling genes) may reflect cardiac stress and an adaptative response to cardiac inflammation, stress and/or injury, after high fat programming. Diet and the sex are determinants of cardiac physiology and pathophysiology, reflecting divergent mechanisms that are sex-specific.

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