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Published on: January 4, 2018
Hypothyroidism compromises hypothalamic leptin signaling in mice.
Claudia Groba1, Steffen Mayerl, Alies A van Mullem
1Leibniz Institute for Age Research/Fritz Lipmann Institute e.V., Beutenbergstr. 11, D-07745 Jena/Germany.
Molecular Endocrinology (Baltimore, Md.)
|March 23, 2013
Summary
Thyroid hormone (TH) impacts metabolism. Hypothyroidism impairs leptin signaling in the brain, affecting energy balance and nutritional sensing.
Area of Science:
- Endocrinology
- Neuroscience
- Metabolism
Background:
- Thyroid hormone (TH) is crucial for metabolism and energy expenditure.
- The role of TH in central nervous system nutritional sensing is not well understood.
Purpose of the Study:
- To investigate the effects of hypothyroidism on leptin production and central leptin sensing.
- To elucidate the impact of thyroid hormone receptor 1 (Trhr1) deficiency on leptin signaling.
Main Methods:
- Studied congenital hypothyroid TRH receptor 1 knockout (Trhr1 ko) mice and euthyroid controls.
- Generated hypothyroid and leptin-deficient mice by crossing Trhr1 ko with leptin-deficient ob/ob mice.
- Assessed leptin levels, leptin receptor expression, STAT3 activation, and SOCS3 levels.
Main Results:
- Hypothyroid mice had lower circulating leptin due to reduced fat mass and adipose tissue expression.
- Hypothyroid mice exhibited increased hypothalamic leptin receptor (Ob-R) expression and decreased suppressor of cytokine signaling 3 (SOCS3) transcript levels.
- Hypothyroid/leptin-deficient mice showed blunted responses to leptin treatment, with altered STAT3 activation and SOCS3 levels in the arcuate nucleus.
Conclusions:
- Hypothyroidism alters intracellular processing of leptin signals in the central nervous system.
- Thyroid hormone influences energy metabolism through a novel mechanism involving leptin signaling pathways.
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