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

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.

Fatty Liver Is a Better Marker of Muscle Insulin Resistance than Visceral Fat Accumulation in Nonobese Japanese Men

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1854-P
Author(s):  
SATOSHI KADOWAKI ◽  
YOSHIFUMI TAMURA ◽  
YUKI SOMEYA ◽  
KAGEUMI TAKENO ◽  
TAKASHI FUNAYAMA ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Liver ◽  
Visceral Fat ◽  
Japanese Men ◽  
Muscle Insulin Resistance ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

Cut-Off Points of Visceral Fat Area Associated with the Risk of Insulin Resistance in Pediatric Practice

Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154613
Author(s):  
Daria Podchinenova ◽  
Julia Samoilova ◽  
Oxana Oleynik ◽  
Maria Matveeva
Keyword(s):  
Insulin Resistance ◽  
Visceral Fat ◽  
Pediatric Practice ◽  
Visceral Fat Area

scholarly journals Influence of methyltestosterone postmenopausal therapy on plasma lipids, inflammatory factors, glucose metabolism and visceral fat: a randomized study

2006 ◽  
Vol 154 (1) ◽  
pp. 131-139 ◽  
Author(s):  
Lenora M Camarate S M Leão ◽  
Mônica Peres C Duarte ◽  
Dalva Margareth B Silva ◽  
Paulo Roberto V Bahia ◽  
Cláudia Medina Coeli ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factors ◽  
Postmenopausal Women ◽  
Fat Mass ◽  
Visceral Fat ◽  
Increased Risk

Background: There has been a growing interest in treating postmenopausal women with androgens. However, hyperandrogenemia in females has been associated with increased risk of cardiovascular disease. Objective: We aimed to assess the effects of androgen replacement on cardiovascular risk factors. Design: Thirty-seven postmenopausal women aged 42–62 years that had undergone hysterectomy were prospectively enrolled in a double-blind protocol to receive, for 12 months, percutaneous estradiol (E2) (1 mg/day) combined with either methyltestosterone (MT) (1.25 mg/day) or placebo. Methods: Along with treatment, we evaluated serum E2, testosterone, sex hormone-binding globulin (SHBG), free androgen index, lipids, fibrinogen, and C-reactive protein; glucose tolerance; insulin resistance; blood pressure; body-mass index; and visceral and subcutaneous abdominal fat mass as assessed by computed tomography. Results: A significant reduction in SHBG (P < 0.001) and increase in free testosterone index (P < 0.05; Repeated measures analysis of variance) were seen in the MT group. Total cholesterol, triglycerides, fibrinogen, and systolic and diastolic blood pressure were significantly lowered to a similar extent by both regimens, but high-density lipoprotein cholesterol decreased only in the androgen group. MT-treated women showed a modest rise in body weight and gained visceral fat mass relative to the other group (P < 0.05), but there were no significant detrimental effects on fasting insulin levels and insulin resistance. Conclusion: This study suggests that the combination of low-dose oral MT and percutaneous E2, for 1 year, does not result in expressive increase of cardiovascular risk factors. This regimen can be recommended for symptomatic postmenopausal women, although it seems prudent to perform baseline and follow-up lipid profile and assessment of body composition, especially in those at high risk of cardiovascular disease.

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

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

2007 ◽  
Vol 292 (3) ◽  
pp. E654-E667 ◽  
Author(s):  
Dake Qi ◽  
Brian Rodrigues
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Glucose Utilization ◽  
Experimental Studies ◽  
Cardiac Metabolism ◽  
Multiple Organ ◽  
Whole Body ◽  
Metabolic Abnormalities ◽  
Organ Systems ◽  
Per Se

Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in “lipotoxicity”. In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease.

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
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