Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 31, Pages 12587-12594Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0705408104
Keywords
type 2 diabetes; nonalcoholic fatty liver disease; adipocytokines; abdominal obesity; atherogenic dyslipidemia
Categories
Funding
- NCRR NIH HHS [M01 RR000125, M01 RR 00125] Funding Source: Medline
- NIA NIH HHS [R01 AG023686, R01 AG 23686] Funding Source: Medline
- NIBIB NIH HHS [R01 EB006494, R01 EB 006494] Funding Source: Medline
- NIDDK NIH HHS [P30 DK045735, R01 DK 43051, R01 DK043051, P01 DK 068229, P30 DK 45735, P01 DK068229] Funding Source: Medline
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We examined the hypothesis that insulin resistance in skeletal muscle promotes the development of atherogenic dyslipidemia, associated with the metabolic syndrome, by altering the distribution pattern of postprandial energy storage. Following ingestion of two high carbohydrate mixed meals, net muscle glycogen synthesis was reduced by approximate to 60% in young, lean, insulin-resistant subjects compared with a similar cohort of age-weight-body mass inclex-activity- matched, insulin-sensitive, control subjects. In contrast, hepatic de novo, lipogenesis and hepatic triglyceride synthesis were both increased by > 2-fold in the insulin-resistant subjects. These changes were associated with a 60% increase in plasma triglyceride concentrations and an approximate to 20% reduction in plasma high-density lipoprotein concentrations but no differences in plasma concentrations of TNF-alpha, IL-6, adiponectin, resistin, retinol binding protein-4, or intraabdominal fat volume. These data demonstrate that insulin resistance in skeletal muscle, due to decreased muscle glycogen synthesis, can promote atherogenic dyslipidemia by changing the pattern of ingested carbohydrate away from skeletal muscle glycogen synthesis into hepatic de novo lipogenesis, resulting in an increase in plasma triglyceride concentrations and a reduction in plasma high-density lipoprotein concentrations. Furthermore, insulin resistance in these subjects was independent of changes in the plasma concentrations of TNF-alpha, IL-6, high-molecular-weight adiponectin, resistin, retinol binding protein-4, or intraabdominal obesity, suggesting that these factors do not play a primary role in causing insulin resistance in the early stages of the metabolic syndrome.
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