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Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals.
Am J Clin Nutr. 2008 Feb; 87(2):295-302.AJ

Abstract

BACKGROUND

Enlargement of adipocytes from subcutaneous abdominal adipose tissue (SAT), increased intrahepatic lipid content (IHL), intramyocellular lipid content (IMCL), and low circulating adiponectin concentrations are associated with insulin resistance.

OBJECTIVE

Because adiponectin increases fat oxidation in skeletal muscle and liver, and the expression of the adiponectin gene in SAT is inversely associated with adipocyte size, we hypothesized that hypoadiponectinemia links hypertrophic obesity with insulin resistance via increased IMCL and IHL.

DESIGN

Fifty-three obese Pima Indians with a mean (+/-SD) age of 27 +/- 8 y, body fat of 35 +/- 5%, and normal glucose regulation (normal fasting and 2-h glucose concentration per WHO 1999 criteria) underwent euglycemic-hyperinsulinemic clamp, biopsies of SAT and vastus lateralis muscle, and magnetic resonance imaging of the abdomen.

RESULTS

Adipocyte diameter (AD) correlated positively with body fat (P < 0.0001) and IHL (estimated from magnetic resonance imaging intensity of liver; P = 0.047). No association was found between AD and plasma adiponectin or IMCL. Plasma adiponectin negatively correlated with type II IMCL (IIA, P = 0.004; IIX, P = 0.009) or IHL (P = 0.02). In a multivariate analysis, plasma adiponectin, AD, and visceral adipose tissue (VAT) independently predicted IHL. Low insulin-mediated glucose disposal was associated with low plasma adiponectin (P = 0.02) and high IHL (P = 0.0003), SAT (P = 0.02), and VAT (P = 0.04). High IHL was the only predictor of reduced insulin-mediated suppression of hepatic glucose production (P = 0.02) and the only independent predictor of insulin-mediated glucose disposal in a multivariate analysis.

CONCLUSIONS

Increased lipid content in the liver may independently link hypoadiponectinemia, hypertrophic obesity, and increased visceral adiposity with peripheral and hepatic insulin resistance.

Authors+Show Affiliations

Obesity and Diabetes Clinical Research Section, NIDDK/NIH/DHHS, Phoenix, AZ 85016, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18258617

Citation

Koska, Juraj, et al. "Increased Fat Accumulation in Liver May Link Insulin Resistance With Subcutaneous Abdominal Adipocyte Enlargement, Visceral Adiposity, and Hypoadiponectinemia in Obese Individuals." The American Journal of Clinical Nutrition, vol. 87, no. 2, 2008, pp. 295-302.
Koska J, Stefan N, Permana PA, et al. Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals. Am J Clin Nutr. 2008;87(2):295-302.
Koska, J., Stefan, N., Permana, P. A., Weyer, C., Sonoda, M., Bogardus, C., Smith, S. R., Joanisse, D. R., Funahashi, T., Krakoff, J., & Bunt, J. C. (2008). Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals. The American Journal of Clinical Nutrition, 87(2), 295-302.
Koska J, et al. Increased Fat Accumulation in Liver May Link Insulin Resistance With Subcutaneous Abdominal Adipocyte Enlargement, Visceral Adiposity, and Hypoadiponectinemia in Obese Individuals. Am J Clin Nutr. 2008;87(2):295-302. PubMed PMID: 18258617.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals. AU - Koska,Juraj, AU - Stefan,Norbert, AU - Permana,Paska A, AU - Weyer,Christian, AU - Sonoda,Mina, AU - Bogardus,Clifton, AU - Smith,Steven R, AU - Joanisse,Denis R, AU - Funahashi,Tohru, AU - Krakoff,Jonathan, AU - Bunt,Joy C, PY - 2008/2/9/pubmed PY - 2008/3/26/medline PY - 2008/2/9/entrez SP - 295 EP - 302 JF - The American journal of clinical nutrition JO - Am. J. Clin. Nutr. VL - 87 IS - 2 N2 - BACKGROUND: Enlargement of adipocytes from subcutaneous abdominal adipose tissue (SAT), increased intrahepatic lipid content (IHL), intramyocellular lipid content (IMCL), and low circulating adiponectin concentrations are associated with insulin resistance. OBJECTIVE: Because adiponectin increases fat oxidation in skeletal muscle and liver, and the expression of the adiponectin gene in SAT is inversely associated with adipocyte size, we hypothesized that hypoadiponectinemia links hypertrophic obesity with insulin resistance via increased IMCL and IHL. DESIGN: Fifty-three obese Pima Indians with a mean (+/-SD) age of 27 +/- 8 y, body fat of 35 +/- 5%, and normal glucose regulation (normal fasting and 2-h glucose concentration per WHO 1999 criteria) underwent euglycemic-hyperinsulinemic clamp, biopsies of SAT and vastus lateralis muscle, and magnetic resonance imaging of the abdomen. RESULTS: Adipocyte diameter (AD) correlated positively with body fat (P < 0.0001) and IHL (estimated from magnetic resonance imaging intensity of liver; P = 0.047). No association was found between AD and plasma adiponectin or IMCL. Plasma adiponectin negatively correlated with type II IMCL (IIA, P = 0.004; IIX, P = 0.009) or IHL (P = 0.02). In a multivariate analysis, plasma adiponectin, AD, and visceral adipose tissue (VAT) independently predicted IHL. Low insulin-mediated glucose disposal was associated with low plasma adiponectin (P = 0.02) and high IHL (P = 0.0003), SAT (P = 0.02), and VAT (P = 0.04). High IHL was the only predictor of reduced insulin-mediated suppression of hepatic glucose production (P = 0.02) and the only independent predictor of insulin-mediated glucose disposal in a multivariate analysis. CONCLUSIONS: Increased lipid content in the liver may independently link hypoadiponectinemia, hypertrophic obesity, and increased visceral adiposity with peripheral and hepatic insulin resistance. SN - 0002-9165 UR - https://www.unboundmedicine.com/medline/citation/18258617/Increased_fat_accumulation_in_liver_may_link_insulin_resistance_with_subcutaneous_abdominal_adipocyte_enlargement_visceral_adiposity_and_hypoadiponectinemia_in_obese_individuals_ L2 - https://academic.oup.com/ajcn/article-lookup/doi/10.1093/ajcn/87.2.295 DB - PRIME DP - Unbound Medicine ER -