The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss
Abstract
The current study was undertaken to investigate fatty acid metabolism by skeletal muscle to examine potential mechanisms that could lead to increased muscle triglyceride in obesity. Sixteen lean and 40 obese research volunteers had leg balance measurement of glucose and free fatty acid (FFA) uptake (fractional extraction of [9,10 (3)H]oleate) and indirect calorimetry across the leg to determine substrate oxidation during fasting and insulin-stimulated conditions. Muscle obtained by percutaneous biopsy had lower carnitine palmitoyl transferase (CPT) activity and oxidative enzyme activity in obesity (P < 0.05). During fasting conditions, obese subjects had an elevated leg respiratory quotient (RQ, 0.83 +/- 0.02 vs. 0.90 +/- 0.01; P < 0.01) and reduced fat oxidation but similar FFA uptake across the leg. During insulin infusions, fat oxidation by leg tissues was suppressed in lean but not obese subjects; rates of FFA uptake were similar. Fasting values for leg RQ correlated with insulin sensitivity (r = -0.57, P < 0.001). Thirty-two of the obese subjects were restudied after weight loss (WL, -14.0 +/- 0.9 kg); insulin sensitivity and insulin suppression of fat oxidation improved (P < 0.01), but fasting leg RQ (0.90 +/- 0.02 vs. 0.90 +/- 0.02, pre-WL vs. post-WL) and muscle CPT activity did not change. The findings suggest that triglyceride accumulation in skeletal muscle in obesity derives from reduced capacity for fat oxidation and that inflexibility in regulating fat oxidation, more than fatty acid uptake, is related to insulin resistance.
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In the citing paper
“In those studies, insulin-resistant states are clearly associated with impaired metabolic flexibility to glucose (MetFlex-glu).”
From Metabolic flexibility to lipid availability during exercise is enhanced in individuals with high insulin sensitivity (2018) · cites this paper as [18]
In the citing paper
“Consequently, reduced mitochondrial oxidative capacity further impairs skeletal muscle oxidation, contributing to the development of insulin resistance commonly associated with obese individuals [53].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [53]
In the citing paper
“Several studies have reported decreased fat oxidation in skeletal muscle, independent of the plasma FFA concentration [100–102].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [100]
In the citing paper
“In one study that compared muscle fat oxidation across the leg in obese (BMI = 34 kg/m2) compared to lean (BMI = 23 kg/m2) individuals, the rate of fatty acid oxidation was reduced in the obese group despite similar arterial FFA concentrations [100].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [100]
In the citing paper
“The metabolic flexibility assessed by the ability to switch from fat to carbohydrate oxidation is usually impaired during a hyperinsulinemic clamp in insulin-resistant subjects; however, this “metabolic inflexibility” is mostly the consequence of impaired cellular glucose uptake.”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [24]
In the citing paper
“Metabolic inflexibility to glucose and impaired glucose storage during a hyperinsulinemic clamp is consistently reported in insulin-resistant subjects.”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [24]
In the citing paper
“In fact, a direct relationship between metabolic flexibility to glucose and glucose disposal rate is described ([14](#r14), [24](#r24), [61](#r61), [62](#r62)) ([Fig. 3*B*](#f3)).”
From Metabolic flexibility and insulin resistance (2008) · cites this paper as [24]
In the citing paper
“This results in defective oxidative metabolism and impaired ability to completely oxidize fatty acid thus favoring the intramyocellular accumulation of lipotoxic lipid species and metabolites derived from the incomplete oxidation of fatty acids which hamper insulin signaling.[130][131][132]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [130]
In the citing paper
“Mitochondrial dysfunction has been implicated in the pathogenesis of insulin resistance, the hallmark of type 2 diabetes mellitus (T2DM).”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Kelley et al., 1999
In the citing paper
“The preliminary evidence linking mitochondrial dysfunction to insulin resistance comes from studies performed in obese and insulin-resistant individuals who exhibited a decrease in skeletal muscle mitochondria oxidative capacity and defective lipid metabolism compared to healthy, lean controls (Kelley et al., 1999; Simoneau et al., 1999; Kim et al., 2000a).”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Kelley et al., 1999
In the citing paper
“which in turn has been described as a pivotal metabolic defect in obesity and insulin resistance (Kelley et al., 1999; Simoneau et al., 1999)”
From Mitochondrial (Dys)function and Insulin Resistance: From Pathophysiological Molecular Mechanisms to the Impact of Diet (2019) · cites this paper as Kelley et al., 1999
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Metadata
- Authors
- Kelley, D. E., Goodpaster, B., Wing, R. R., & Simoneau, J.-A.
- Affiliations
- Pediatrics and Genetics (US)
- University of Pittsburgh (US)
- Division of Kinesiology, Department of Social and Preventive Medicine, Laval University, Ste-Foy, Quebec, Canada G1K 7P4
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 1999-12-01
- Volume
- 277
- Issue
- 6
- Pages
- E1130-E1141
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2216710583
- Cited by
- 1,096
- References
- 60
- Citations by year
- 2026: 13 · 2025: 39 · 2024: 34 · 2023: 43 · 2022: 43 · 2021: 50 · 2020: 45 · 2019: 48 · 2018: 46 · 2017: 41 · 2016: 38 · 2015: 39 · 2014: 40 · 2013: 54 · 2012: 48
- FWCI
- 9.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p30dk046204-15)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK49200-02, 1P30DK-46204, R01DK049200)
- National Center for Research Resources (M01RR000056)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- insulin resistance, obesity, weight loss, fat oxidation, free fatty acid uptake, carnitine palmitoyltransferase, respiratory quotient, insulin sensitivity, substrate oxidation
- MeSH terms
- Adult, Arteries, Blood Glucose, Calorimetry, Indirect, Diet, Reducing, Postural Balance, Fasting, Fatty Acids, Female, Glucose, Humans, Hypoglycemic Agents, Insulin, Insulin Resistance, Leg, Male, Middle Aged, Obesity, Veins, Weight Loss, Muscle, Skeletal
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