Journal
ANNUAL REVIEW OF PHYSIOLOGY
Volume 72, Issue -, Pages 219-246Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev-physiol-021909-135846
Keywords
obesity; adipose tissue; skeletal muscle; Kupffer cell
Categories
Funding
- National Institution of Health [DK033651, DK074868, T32 OK 007494, DK063491]
- Eunice Kennedy Shriver NICHD/NTH [U54 HD 012303-25]
- Leducq Foundation Transatlantic Network
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [U54HD012303, P50HD012303] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK063491, P01DK074868, R37DK033651, R01DK033651, T32DK007494] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Obesity induces an insulin-resistant state in adipose tissue, liver, and muscle and is a strong risk factor for the development of type 2 diabetes mellitus. Insulin resistance in the setting of obesity results from a combination of altered functions of insulin target cells and the accumulation of macrophages that secrete proinflammatory mediators. At the molecular level, insulin resistance is promoted by a transition in macrophage polarization from an alternative M2 activation state maintained by STAT6 and PPA.Rs to a classical M1 activation state driven by NE-kappa B, AP1, and other signal-dependent transcription factors that play crucial roles in innate immunity. Strategies focused on inhibiting the inflammation/insulin resistance axis that otherwise preserve essential innate immune functions may hold promise for therapeutic intervention.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available