scholarly journals Plasma ferritin concentration is positively associated with in vivo fatty acid mobilization and insulin resistance in obese women

2018 ◽  
Vol 103 (11) ◽  
pp. 1443-1447 ◽  
Author(s):  
Benjamin J. Ryan ◽  
Douglas W. Van Pelt ◽  
Lisa M. Guth ◽  
Alison C. Ludzki ◽  
Rachel A. Gioscia-Ryan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Obese Women ◽  
Ferritin Concentration ◽  
Fatty Acid Mobilization

scholarly journals A longitudinal study of the antilipolytic effect of insulin in women following bariatric surgery

2021 ◽  
Author(s):  
Kelvin Ho Man Kwok ◽  
Daniel P. Andersson ◽  
Mikael Rydén ◽  
Peter Arner
Keyword(s):  
Insulin Resistance ◽  
Bariatric Surgery ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Glucose Utilization ◽  
Obese Women ◽  
Fatty Acid Utilization ◽  
Sensitivity Changes ◽  
Gastric By Pass

AbstractInsulin resistance of glucose utilization is fully restored following BMI normalization after bariatric surgery. We investigated if this also pertains to insulin-induced effects on fatty acid handling. Forty-three women with obesity (OB) were investigated before and 2 years after Roux-en-Y gastric by-pass when BMI was <30 kg/m2 (PO) and compared with 26 never obese women (NO). The Adipo-IR index was used as measure of insulin antilipolytic sensitivity. Changes (delta) in circulating glycerol and fatty acid levels during hyperinsulinemic euglycemic clamp represented the insulin maximum antilipolytic effect. Overall fatty acid utilization was reflected by delta fatty acids minus 3 × delta glycerol. Adipo-IR was higher in OB than in NO and PO (p < 0.0001), the latter two groups having similar values. Insulin lowered glycerol levels by about 70% in all groups, but delta glycerol was 30% larger in PO than in NO (p = 0.04). Delta adds and adds utilization were similar in all groups. We conclude that women with obesity, whose BMI is normalized after bariatric surgery, have improved maximum in vivo antilipolytic effect of insulin above expected in absolute but not relative terms as regards glycerol changes, while the handling of circulating fatty acids is changed to the normal state.

Insulin Resistance and In Vivo Lipolytic Rate Are Positively Associated with Body Iron Stores in Obese Women

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2048-P
Author(s):  
BENJAMIN J. RYAN ◽  
DOUGLAS W. VAN PELT ◽  
LISA M. GUTH ◽  
ALISON LUDZKI ◽  
RACHEL A. GIOSCIA-RYAN ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Obese Women ◽  
Body Iron ◽  
Iron Stores

Involvement of non-esterified fatty acid oxidation in glucocorticoid-induced peripheral insulin resistance in vivo in rats

Diabetologia ◽  
1993 ◽  
Vol 36 (10) ◽  
pp. 899-906 ◽  
Author(s):  
C. Guillaume-Gentil ◽  
F. Assimacopoulos-Jeannet ◽  
B. Jeanrenaud
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Peripheral Insulin Resistance

scholarly journals Relatively low endogenous fatty acid mobilization and uptake helps preserve insulin sensitivity in obese women

2014 ◽  
Vol 39 (1) ◽  
pp. 149-155 ◽  
Author(s):  
D W Van Pelt ◽  
S A Newsom ◽  
S Schenk ◽  
J F Horowitz
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Obese Women ◽  
Endogenous Fatty Acid ◽  
Fatty Acid Mobilization

100th Anniversary of the discovery of insulin Perspective: Insulin and Adipose Tissue Fatty Acid Metabolism

2021 ◽  
Author(s):  
André C. Carpentier
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Dietary Fatty Acids ◽  
Nonesterified Fatty Acid ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

Insulin inhibits systemic nonesterified fatty acid (NEFA) flux to a greater degree than glucose or any other metabolite. This remarkable effect is mainly due to insulin-mediated inhibition of intracellular triglyceride (TG) lipolysis in adipose tissues and is essential to prevent diabetic ketoacidosis, but also to limit the potential lipotoxic effects of NEFA in lean tissues that contributes to the development of diabetes complications. Insulin also regulates adipose tissue fatty acid esterification, glycerol and TG synthesis, lipogenesis and possibly oxidation, contributing to the trapping of dietary fatty acids in the postprandial state. Excess NEFA flux at a given insulin level has been used to define in vivo adipose tissue insulin resistance. Adipose tissue insulin resistance defined in this fashion has been associated with several dysmetabolic features and complications of diabetes, but the mechanistic significance of this concept is not fully understood. This review focusses on the in vivo regulation of adipose tissue fatty acid metabolism by insulin and the mechanistic significance of the current definition of adipose tissue insulin resistance. One hundred years after the discovery of insulin and despite decades of investigations, much is still to be understood about the multifaceted in vivo actions of this hormone on adipose tissue fatty acid metabolism.

scholarly journals Peroxisome Proliferator-Activated Receptor (PPAR) Activation Induces Tissue-Specific Effects on Fatty Acid Uptake and Metabolism in Vivo—A Study Using the Novel PPARα/γ Agonist Tesaglitazar

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3158-3164 ◽  
Author(s):  
Bronwyn D. Hegarty ◽  
Stuart M. Furler ◽  
Nicholas D. Oakes ◽  
Edward W. Kraegen ◽  
Gregory J. Cooney
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Insulin Action ◽  
Whole Body ◽  
Peroxisome Proliferator ◽  
The Novel ◽  
High Fat

Abstract Agonists of peroxisome proliferator-activated receptors (PPARs) have emerged as important pharmacological agents for improving insulin action. A major mechanism of action of PPAR agonists is thought to involve the alteration of the tissue distribution of nonesterified fatty acid (NEFA) uptake and utilization. To test this hypothesis directly, we examined the effect of the novel PPARα/γ agonist tesaglitazar on whole-body insulin sensitivity and NEFA clearance into epididymal white adipose tissue (WAT), red gastrocnemius muscle, and liver in rats with dietary-induced insulin resistance. Wistar rats were fed a high-fat diet (59% of calories as fat) for 3 wk with or without treatment with tesaglitazar (1 μmol·kg−1·d−1, 7 d). NEFA clearance was measured using the partially metabolizable NEFA tracer, 3H-R-bromopalmitate, administered under conditions of basal or elevated NEFA availability. Tesaglitazar improved the insulin sensitivity of high-fat-fed rats, indicated by an increase in the glucose infusion rate during hyperinsulinemic-euglycemic clamp (P &lt; 0.01). This improvement in insulin action was associated with decreased diglyceride (P &lt; 0.05) and long chain acyl coenzyme A (P &lt; 0.05) in skeletal muscle. NEFA clearance into WAT of high-fat-fed rats was increased 52% by tesaglitazar under basal conditions (P &lt; 0.001). In addition the PPARα/γ agonist moderately increased hepatic and muscle NEFA utilization and reduced hepatic triglyceride accumulation (P &lt; 0.05). This study shows that tesaglitazar is an effective insulin-sensitizing agent in a mild dietary model of insulin resistance. Furthermore, we provide the first direct in vivo evidence that an agonist of both PPARα and PPARγ increases the ability of WAT, liver, and skeletal muscle to use fatty acids in association with its beneficial effects on insulin action in this model.

Adipocyte fatty acid mobilization in vivo: Effects of age and anatomical location

Lipids ◽  
1985 ◽  
Vol 20 (5) ◽  
pp. 255-261 ◽  
Author(s):  
Arthur D. Hartman
Keyword(s):  
Fatty Acid ◽  
Anatomical Location ◽  
In Vivo Effects ◽  
Fatty Acid Mobilization

Impaired insulin action in subcutaneous adipocytes from women with visceral obesity

2001 ◽  
Vol 280 (1) ◽  
pp. E40-E49 ◽  
Author(s):  
Julia A. Johnson ◽  
Susan K. Fried ◽  
F. Xavier Pi-Sunyer ◽  
Jeanine B. Albu
Keyword(s):  
Insulin Resistance ◽  
Visceral Obesity ◽  
Nonesterified Fatty Acid ◽  
Obese Women ◽  
Black And White ◽  
Adenosine Receptor Agonist ◽  
Impaired Insulin Action ◽  
Visceral Adipose

Visceral obesity is associated with resistance to the antilipolytic effect of insulin in vivo. We investigated whether subcutaneous abdominal and gluteal adipocytes from viscerally obese women exhibit insulin resistance in vitro. Subjects were obese black and white premenopausal nondiabetic women matched for visceral adipose tissue (VAT), total adiposity, and age. Independently of race and adipocyte size, increased VAT was associated with decreased sensitivity to insulin's antilipolytic effect in subcutaneous abdominal and gluteal adipocytes. Absolute lipolytic rates at physiologically relevant concentrations of insulin or the adenosine receptor agonist N 6-(phenylisopropyl)adenosine were higher in subjects with the highest vs. lowest VAT area. Independently of cell size, abdominal adipocytes were less sensitive to the antilipolytic effect of insulin than gluteal adipocytes, which may partly explain increased nonesterified fatty acid fluxes in upper vs. lower body obese women. Moreover, increased VAT was associated with decreased responsiveness, but not decreased sensitivity, to insulin's stimulatory effect on glucose transport in abdominal adipocytes. These data suggest that insulin resistance of subcutaneous abdominal and, to a lesser extent, gluteal adipocytes may contribute to increased systemic lipolysis in both black and white viscerally obese women.

scholarly journals Higher Fasting and Postprandial Free Fatty Acid Levels Are Associated With Higher Muscle Insulin Resistance and Lower Insulin Secretion in Young Non-Obese Women

2018 ◽  
Vol 10 (11) ◽  
pp. 822-829
Author(s):  
Mika Takeuchi ◽  
Satomi Minato ◽  
Kaori Kitaoka ◽  
Ayaka Tsuboi ◽  
Miki Kurata ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Obese Women ◽  
Muscle Insulin Resistance

Relationship between visceral adiposity and intramyocellular lipid content in two rat models of insulin resistance

2005 ◽  
Vol 288 (1) ◽  
pp. E106-E116 ◽  
Author(s):  
M. Korach-André ◽  
J. Gao ◽  
J. S. Gounarides ◽  
R. Deacon ◽  
A. Islam ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Visceral Fat ◽  
Visceral Adiposity ◽  
Zucker Rats ◽  
Intramyocellular Lipid ◽  
Dexamethasone Treatment ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation

High visceral adiposity and intramyocellular lipid levels (IMCL) are both associated with the development of type 2 diabetes. The relationship between visceral adiposity and IMCL levels was explored in diet- and glucocorticoid-induced models of insulin resistance. In the diet-induced model, lean and fa/fa Zucker rats were fed either normal or high-fat (HF) chow over 4 wk. Fat distribution, IMCL content in the tibialis anterior (TA) muscle (IMCLTA), and whole body insulin resistance were measured before and after the 4-wk period. The HF diet-induced increase in IMCLTA was strongly correlated with visceral fat accumulation and greater glucose intolerance in both groups. The increase in IMCLTA to visceral fat accumulation was threefold greater for fa/fa rats. In the glucocorticoid-induced model, insulin sensitivity was impaired with dexamethasone. In vivo adiposity and IMCLTA content measurements were combined with ex vivo analysis of plasma and muscle tissue. Dexamethasone treatment had minimal effects on visceral fat accumulation while increasing IMCLTA levels ∼30% ( P < 0.05) compared with controls. Dexamethasone increased plasma glucose by twofold and increased the saturated fatty acid content of plasma lipids [fatty acid (CH2) n/ωCH3 ratio +15%, P < 0.05]. The lipid composition of the TA muscle was unchanged by dexamethasone treatment, indicating that the relative increase in IMCLTA observed in vivo resulted from a decrease in lipid oxidation. Visceral adiposity may influence IMCL accumulation in the context of dietary manipulations; however, a “causal” relationship still remains to be determined. Dexamethasone-induced insulin resistance likely operates under a different mechanism, i.e., independently of visceral adiposity.

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