scholarly journals Commentary on: Increase in visceral fatper sedoes not induce insulin resistance in the canine model

Obesity ◽  
2014 ◽  
Vol 23 (1) ◽  
pp. 4-4
Author(s):  
Jose E. Galgani ◽  
Cedric Moro
Keyword(s):  
Insulin Resistance ◽  
Canine Model ◽  
Induce Insulin Resistance

scholarly journals Lipid-induced insulin resistance does not impair insulin access to skeletal muscle

2015 ◽  
Vol 308 (11) ◽  
pp. E1001-E1009 ◽  
Author(s):  
Cathryn M. Kolka ◽  
Joyce M. Richey ◽  
Ana Valeria B. Castro ◽  
Josiane L. Broussard ◽  
Viorica Ionut ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Fold Increase ◽  
Canine Model ◽  
Hepatic Insulin Resistance ◽  
Lipid Infusion ◽  
Peripheral Insulin Resistance ◽  
Induce Insulin Resistance

Elevated plasma free fatty acids (FFA) induce insulin resistance in skeletal muscle. Previously, we have shown that experimental insulin resistance induced by lipid infusion prevents the dispersion of insulin through the muscle, and we hypothesized that this would lead to an impairment of insulin moving from the plasma to the muscle interstitium. Thus, we infused lipid into our anesthetized canine model and measured the appearance of insulin in the lymph as a means to sample muscle interstitium under hyperinsulinemic euglycemic clamp conditions. Although lipid infusion lowered the glucose infusion rate and induced both peripheral and hepatic insulin resistance, we were unable to detect an impairment of insulin access to the lymph. Interestingly, despite a significant, 10-fold increase in plasma FFA, we detected little to no increase in free fatty acids or triglycerides in the lymph after lipid infusion. Thus, we conclude that experimental insulin resistance induced by lipid infusion does not reduce insulin access to skeletal muscle under clamp conditions. This would suggest that the peripheral insulin resistance is likely due to reduced cellular sensitivity to insulin in this model, and yet we did not detect a change in the tissue microenvironment that could contribute to cellular insulin resistance.

scholarly journals Increase in visceral fat per se does not induce insulin resistance in the canine model

Obesity ◽  
2014 ◽  
Vol 23 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Ana V.B. Castro ◽  
Orison O. Woolcott ◽  
Malini S. Iyer ◽  
Morvarid Kabir ◽  
Viorica Ionut ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Visceral Fat ◽  
Canine Model ◽  
Induce Insulin Resistance ◽  
Per Se

Transferrin and iron induce insulin resistance of glucose transport in adipocytes

Metabolism ◽  
2006 ◽  
Vol 55 (8) ◽  
pp. 1042-1045 ◽  
Author(s):  
Allan Green ◽  
Robin Basile ◽  
John M. Rumberger
Keyword(s):  
Insulin Resistance ◽  
Glucose Transport ◽  
Induce Insulin Resistance

Lipids activate skeletal muscle mitochondrial fission and quality control networks to induce insulin resistance in humans

Metabolism ◽  
2021 ◽  
pp. 154803
Author(s):  
Christopher L. Axelrod ◽  
Ciaran E. Fealy ◽  
Melissa L. Erickson ◽  
Gangarao Davuluri ◽  
Hisashi Fujioka ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Quality Control ◽  
Mitochondrial Fission ◽  
Control Networks ◽  
Induce Insulin Resistance

scholarly journals Isoflurane and Sevoflurane Induce Severe Hepatic Insulin Resistance in a Canine Model

PLoS ONE ◽  
2016 ◽  
Vol 11 (11) ◽  
pp. e0163275 ◽  
Author(s):  
Stella P. Kim ◽  
Josiane L. Broussard ◽  
Cathryn M. Kolka
Keyword(s):  
Insulin Resistance ◽  
Canine Model ◽  
Hepatic Insulin Resistance

scholarly journals Age and tissue specific differences in the development of acute insulin resistance following injury

2009 ◽  
Vol 203 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Lidong Zhai ◽  
Joseph L Messina
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Signaling ◽  
Intracellular Signaling ◽  
Male Rats ◽  
Hepatic Insulin Resistance ◽  
Surgical Trauma ◽  
Induce Insulin Resistance ◽  
Old Rats ◽  
Effect Of Age

Injuries, hemorrhage, sepsis, burn, and critical illnesses all induce insulin resistance, and insulin resistance is strongly associated with advancing age. However, the effect of age on injury induced insulin resistance is not well studied. We performed surgical trauma in male rats of three different ages (3-, 6-, and 10-weeks old). Rats were either hemorrhaged to a mean arterial pressure of 35–40 mmHg and subsequently maintained at that pressure for up to 90 min, or maintained without hemorrhage as controls. Results indicate that insulin-induced intracellular signaling was diminished in liver and skeletal muscle of 6- and 10-week old rats following trauma and hemorrhage. In even younger rats, immediately post-weaning (∼3 weeks of age), insulin signaling was lost in liver, but not in skeletal muscle. Glucocorticoids can play a role in the chronic development of insulin resistance. Our results demonstrate that corticosterone levels were increased in 6- and 10-week old animals following hemorrhage, but little change was measured in 3-week old animals. Blockade of glucocorticoid synthesis prevented the development of insulin resistance in skeletal muscle, but not in liver of 6- and 10-week old rats. Moreover, skeletal muscle glucocorticoid receptor levels increased dramatically between 3 and 6 weeks of age. These results indicate that trauma and hemorrhage-induced hepatic insulin resistance occurs at all ages tested. However, there is no development of insulin resistance following trauma and hemorrhage in skeletal muscle of post-weaning rats. In skeletal muscle of 6- and 10-week old rats, inhibition of glucocorticoid levels prevents the development of insulin resistance.

scholarly journals Muscle Adaptation to Short-Term Fasting in Healthy Lean Humans

2008 ◽  
Vol 93 (7) ◽  
pp. 2900-2903 ◽  
Author(s):  
Maarten R. Soeters ◽  
Hans P. Sauerwein ◽  
Peter F. Dubbelhuis ◽  
Johanna E. Groener ◽  
Mariëtte T. Ackermans ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Protein Kinase B ◽  
Muscle Adaptation ◽  
Short Term ◽  
Akt Phosphorylation ◽  
Induce Insulin Resistance ◽  
Before And After ◽  
Muscle Biopsies

Abstract Context: It has been demonstrated repeatedly that short-term fasting induces insulin resistance, although the exact mechanism in humans is unknown to date. Intramyocellular sphingolipids (i.e. ceramide) have been suggested to induce insulin resistance by interfering with the insulin signaling cascade in obesity. Objective: Our objective was to study peripheral insulin sensitivity together with muscle ceramide concentrations and protein kinase B/AKT phosphorylation after short-term fasting. Main Outcome Measures and Design: After 14- and 62-h fasting, glucose fluxes were measured before and after a hyperinsulinemic euglycemic clamp. Muscle biopsies were performed in the basal state and during the clamp to assess muscle ceramide and protein kinase B/AKT. Results: Insulin-mediated peripheral glucose uptake was significantly lower after 62-h fasting compared with 14-h fasting. Intramuscular ceramide concentrations tended to increase during fasting. During the clamp the phosphorylation of protein kinase B/AKT at serine473 in proportion to the total amount of protein kinase B/AKT was significantly lower. Muscle ceramide did not correlate with plasma free fatty acids. Conclusions: Fasting for 62 h decreases insulin-mediated peripheral glucose uptake with lower phosphorylation of AKT at serine473. AKT may play a regulatory role in fasting-induced insulin resistance. Whether the decrease in AKT can be attributed to the trend to higher muscle ceramide remains unanswered.

scholarly journals The Liver as an Endocrine Organ—Linking NAFLD and Insulin Resistance

2019 ◽  
Vol 40 (5) ◽  
pp. 1367-1393 ◽  
Author(s):  
Matthew J Watt ◽  
Paula M Miotto ◽  
William De Nardo ◽  
Magdalene K Montgomery
Keyword(s):  
Insulin Resistance ◽  
Lipid Metabolism ◽  
Liver Disorder ◽  
The Body ◽  
Limited Information ◽  
Peripheral Tissues ◽  
Nonalcoholic Fatty Liver ◽  
Induce Insulin Resistance ◽  
Glucose And Lipid Metabolism ◽  
Physiological Processes

AbstractThe liver is a dynamic organ that plays critical roles in many physiological processes, including the regulation of systemic glucose and lipid metabolism. Dysfunctional hepatic lipid metabolism is a cause of nonalcoholic fatty liver disease (NAFLD), the most common chronic liver disorder worldwide, and is closely associated with insulin resistance and type 2 diabetes. Through the use of advanced mass spectrometry “omics” approaches and detailed experimentation in cells, mice, and humans, we now understand that the liver secretes a wide array of proteins, metabolites, and noncoding RNAs (miRNAs) and that many of these secreted factors exert powerful effects on metabolic processes both in the liver and in peripheral tissues. In this review, we summarize the rapidly evolving field of “hepatokine” biology with a particular focus on delineating previously unappreciated communication between the liver and other tissues in the body. We describe the NAFLD-induced changes in secretion of liver proteins, lipids, other metabolites, and miRNAs, and how these molecules alter metabolism in liver, muscle, adipose tissue, and pancreas to induce insulin resistance. We also synthesize the limited information that indicates that extracellular vesicles, and in particular exosomes, may be an important mechanism for intertissue communication in normal physiology and in promoting metabolic dysregulation in NAFLD.

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