Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Apr;19(2):81-7.
doi: 10.1097/MED.0b013e3283514e13.

What causes the insulin resistance underlying obesity?

Olga T Hardy  1 , Michael P Czech, Silvia Corvera
Affiliations
Review

What causes the insulin resistance underlying obesity?

Olga T Hardy et al. Curr Opin Endocrinol Diabetes Obes. 2012 Apr.

Abstract

Purpose of review: The association between obesity and insulin resistance is an area of much interest and enormous public health impact, with hundreds of articles being published in the last year focused on the possible mechanisms that underlie this association. The purpose to this review is to highlight some of the key recent literature with emphasis on emerging concepts.

Recent findings: The specific link between visceral adipose tissue accumulation and insulin resistance continues to be discerned. Visceral adiposity is correlated with accumulation of excess lipid in liver, and results in cell autonomous impairment in insulin signaling. Visceral adipose tissue is also prone to inflammation and inflammatory cytokine production, which also contribute to impairment in insulin signaling. The expansion of visceral adipose tissue and excess lipid accumulation in liver and muscle may result from limited expandability of subcutaneous adipose tissue, due to the properties of its extracellular matrix and capacity for capillary growth.

Summary: Recent studies underscore the need to better understand the mechanisms linking visceral adiposity with liver fat accumulation, the mechanisms by which ectopic fat accumulation cause insulin resistance, and the mechanisms by which the size of adipose tissue depots is determined.

PubMed Disclaimer

Conflict of interest statement

There are no conflicts of interest.

Conflicts of interest

Work in the authors’ laboratories has been supported by grants from the National Institutes of Health DK089101 to SC, DK30898 to MPC and UMASS Center for Clinical and Translational Science to OTH.

Figures

FIGURE 1
FIGURE 1
Potential mechanisms by which visceral adiposity might be related to insulin resistance. Description of each model is in the text.
See this image and copyright information in PMC

References

    1. Reaven GM. Banting lecture role of insulin resistance in human disease. Diabetes. 1988;37:1595–1607. - PubMed
    1. Sims EA, Danforth E., Jr Expenditure and storage of energy in man. J Clin Invest. 1987;79:1019–1025. - PMC - PubMed
    1. Tchoukalova YD, Votruba SB, Tchkonia T, et al. Regional differences in cellular mechanisms of adipose tissue gain with overfeeding. Proc Natl Acad Sci U S A. 2010;107:18226–18231. - PMC - PubMed
    1. Preis SR, Massaro JM, Robins SJ, et al. Abdominal subcutaneous and visceral adipose tissue and insulin resistance in the Framingham heart study. Obesity (Silver Spring) 2010;18:2191–2198. - PMC - PubMed
    1. McLaughlin T, Lamendola C, Liu A, Abbasi F. Preferential fat deposition in subcutaneous versus visceral depots is associated with insulin sensitivity. J Clin Endocrinol Metab. 2011;96:E1756–E1760. Using computerized tomography to quantify adipose depot size, and normalizing for BMI, the data in this study clarify that regional distribution of fat-favoring subcutaneous depots is associated with lower risk for insulin resistance. - PMC - PubMed

Publication types