Horm Metab Res 2015; 47(09): 681-685
DOI: 10.1055/s-0034-1395673
Endocrine Research
© Georg Thieme Verlag KG Stuttgart · New York

Interacting Effects of TSH and Insulin on Human Differentiated Adipocytes

D. Felske
1  Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada
2  Departments of Medicine and of Biochemistry, Microbiology & Immunology, University of Ottawa, Ontario, Canada
,
A. Gagnon
1  Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada
2  Departments of Medicine and of Biochemistry, Microbiology & Immunology, University of Ottawa, Ontario, Canada
,
A. Sorisky
1  Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada
2  Departments of Medicine and of Biochemistry, Microbiology & Immunology, University of Ottawa, Ontario, Canada
› Author Affiliations
Further Information

Publication History

received 24 September 2014

accepted 20 November 2014

Publication Date:
12 December 2014 (eFirst)

Abstract

Subclinical hypothyroidism, characterized by an isolated rise in TSH serum levels with normal thyroid function, is a pro-inflammatory state associated with insulin resistance. Adipocytes express TSH receptors, but it is not known if TSH can directly inhibit insulin signaling. Using primary human differentiated adipocytes, we examined the effects of TSH on insulin-stimulated Akt phosphorylation, and whether conventional PKC (cPKC) were involved. The effect of insulin on TSH-stimulated lipolysis was also investigated. TSH inhibited insulin-stimulated Akt phosphorylation in adipocytes by 54%. TSH activated cPKC, and Gö6976, a PKCα and -β1 inhibitor, prevented the inhibitory effect of TSH on the insulin response. Insulin reduced the ability of TSH to activate cPKC and to stimulate lipolysis.

Our data reveal novel interactions between TSH and insulin. TSH inhibits insulin-stimulated Akt signaling in a cPKC-dependent fashion, whereas insulin blocks TSH-stimulated cPKC activity and lipolysis. TSH and insulin act on differentiated human adipocytes to modulate their respective intracellular signals.