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Effect of a Sustained Reduction in Plasma Free Fatty Acid Concentration on Intramuscular Long-Chain Fatty Acyl-CoAs and Insulin Action in Type 2 Diabetic Patients
Abstract
To investigate the effect of a sustained (7-day) decrease in plasma free fatty acid (FFA) concentrations on insulin action and intramyocellular long-chain fatty acyl-CoAs (LCFA-CoAs), we studied the effect of acipimox, a potent inhibitor of lipolysis, in seven type 2 diabetic patients (age 53 ± 3 years, BMI 30.2 ± 2.0 kg/m2, fasting plasma glucose 8.5 ± 0.8 mmol/l, HbA1c 7.5 ± 0.4%). Subjects received an oral glucose tolerance test (OGTT) and 120-min euglycemic insulin (80 mU/m2 per min) clamp with 3-[3H]glucose/vastus lateralis muscle biopsies to quantitate rates of insulin-mediated whole-body glucose disposal (Rd) and intramyocellular LCFA-CoAs before and after acipimox (250 mg every 6 h for 7 days). Acipimox significantly reduced fasting plasma FFAs (from 563 ± 74 to 230 ± 33 μmol/l; P < 0.01) and mean plasma FFAs during the OGTT (from 409 ± 44 to 184 ± 22 μmol/l; P < 0.01). After acipimox, decreases were seen in fasting plasma insulin (from 78 ± 18 to 42 ± 6 pmol/l; P < 0.05), fasting plasma glucose (from 8.5 ± 0.8 to 7.0 ± 0.5 mmol/l; P < 0.02), and mean plasma glucose during the OGTT (from 14.5 ± 0.8 to 13.0 ± 0.8 mmol/l; P < 0.05). After acipimox, insulin-stimulated Rd increased from 3.3 ± 0.4 to 4.4 ± 0.4 mg · kg−1 · min−1 (P < 0.03), whereas suppression of endogenous glucose production (EGP) was similar and virtually complete during both insulin clamp studies (0.16 ± 0.10 vs. 0.14 ± 0.10 mg · kg−1 · min−1; P > 0.05). Basal EGP did not change after acipimox (1.9 ± 0.2 vs. 1.9 ± 0.2 mg · kg−1 · min−1). Total muscle LCFA-CoA content decreased after acipimox treatment (from 7.26 ± 0.58 to 5.64 ± 0.79 nmol/g; P < 0.05). Decreases were also seen in muscle palmityl CoA (16:0; from 1.06 ± 0.10 to 0.75 ± 0.11 nmol/g; P < 0.05), palmitoleate CoA (16:1; from 0.48 ± 0.05 to 0.33 ± 0.05 nmol/g; P = 0.07), oleate CoA (18:1; from 2.60 ± 0.11 to 1.95 ± 0.31 nmol/g; P < 0.05), linoleate CoA (18:2; from 1.81 ± 0.26 to 1.38 ± 0.18 nmol/g; P = 0.13), and linolenate CoA (18:3; from 0.27 ± 0.03 to 0.19 ± 0.02 nmol/g; P < 0.03) levels after acipimox treatment. Muscle stearate CoA (18:0) did not decrease after acipimox treatment. The increase in Rd correlated strongly with the decrease in muscle palmityl CoA (r = 0.75, P < 0.05), oleate CoA (r = 0.76, P < 0.05), and total muscle LCFA-CoA (r = 0.74, P < 0.05) levels. Plasma adiponectin did not change significantly after acipimox treatment (7.9 ± 1.8 vs. 7.5 ± 1.5 μg/ml). These data demonstrate that the reduction in intramuscular LCFA-CoA content is closely associated with enhanced insulin sensitivity in muscle after a chronic reduction in plasma FFA concentrations in type 2 diabetic patients despite the lack of an effect on plasma adiponectin concentration.
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In the citing paper
“Conversely, reduction of plasma FFA concentration in insulin resistant individuals, for example, type 2 diabetic subjects, augments insulin-stimulated glucose disposal in skeletal muscle [69–72], and the improvement in insulin sensitivity is closely associated with a reduction in intramyocellular FACoA concentration [69].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [69]
In the citing paper
“(ii) the decrease in insulin resistance brought about by reducing the plasma FFA concentration with acipimox in insulin resistant individuals is associated with a reduction in intracellular FACoA content, and the magnitude of decrease in insulin resistance strongly correlates with the decrease in FACoA content [69];”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [69]
In the citing paper
“In contrast, decreasing fatty acid flux in humans via pharmacological inhibition of lipolysis (49) or by discontinuing a lipid-plus-heparin infusion in rats (58) decreases IMTG concentration and/or the accumulation of fatty acid intermediates.”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [49]
In the citing paper
“Further evidence linking fatty acids to insulin sensitivity comes from clinical studies showing that pharmacological inhibition of lipolysis decreases fatty acid levels and rapidly enhances insulin sen-sitivity in diabetic and nondiabetic, lean and obese subjects (48,49).”
From Insulin sensitivity: Modulation by nutrients and inflammation (2008) · cites this paper as [49]
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Metadata
- Authors
- Bajaj, M., Suraamornkul, S., Romanelli, A., Cline, G. W., Mandarino, L. J., Shulman, G. I., & DeFronzo, R. A.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Howard Hughes Medical Institute (US)
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-11-01
- Volume
- 54
- Issue
- 11
- Pages
- 3148-3153
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2160930691
- Cited by
- 181
- References
- 55
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 1 · 2023: 5 · 2022: 10 · 2021: 7 · 2020: 7 · 2019: 4 · 2018: 8 · 2017: 4 · 2016: 5 · 2015: 11 · 2014: 6 · 2013: 9 · 2012: 11
- FWCI
- 8.49
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 45735, DK 24092, DK-068229, P30DK045735, P01DK068229)
- National Center for Research Resources (M01RR01346, M01RR001346)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- type 2 diabetes, plasma free fatty acids, acipimox, lipolysis inhibition, long-chain fatty acyl-CoA, intramyocellular lipid, insulin action, insulin sensitivity, glucose disposal, insulin-stimulated glucose uptake, endogenous glucose production, insulin resistance, hyperinsulinemic-euglycemic clamp, oral glucose tolerance test, fatty acid oxidation
- MeSH terms
- Acyl Coenzyme A, Hypolipidemic Agents, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Female, Glucose Tolerance Test, Humans, Hyperlipidemias, Insulin, Male, Middle Aged, Pyrazines, Muscle, Skeletal, Adiponectin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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