Importance of neural input and thyroid hormones in the control of brown fat atrophy in mice.

Abstract

In euthyroid mice, a 48-h fast caused brown fat (BAT) atrophy characterized by loss of tissue proteins, succinate dehydrogenase (SDH), and a significant reduction in mitochondrial uncoupling protein (UCP) content. Chemical sympathectomy and surgical denervation failed to mimic the changes in BAT protein and SDH contents observed after food deprivation. However, suppression of sympathetic activity could account for the loss of UCP from the mitochondria. In mice made hyperthyroid by repeated triiodothyronine injections, losses of tissue SDH and proteins caused by food deprivation or surgical denervation were markedly suppressed, while the loss of UCP from the mitochondria remained unchanged. These results suggest that reduced sympathetic activity to BAT in fasted mice is not the exclusive cause of the tissue atrophy and that thyroid hormones may play a role in the control of brown fat atrophy in mice.

• Authors: M Desautels, R A Dulos
• Journal: Canadian journal of physiology and pharmacology (Can J Physiol Pharmacol) Vol. 68 Issue 8 Pg. 1100-7 (Aug 1990) ISSN: 0008-4212 [Print] Canada
• PMID: 2390738 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Thyroid Hormones
• Guanosine Diphosphate
• Succinate Dehydrogenase

Topics

• Adipose Tissue, Brown (drug effects, innervation, pathology)
• Animals
• Atrophy
• Body Weight (drug effects)
• Denervation
• Energy Metabolism (drug effects)
• Food Deprivation (physiology)
• Guanosine Diphosphate (pharmacology)
• Male
• Mice
• Mice, Inbred Strains
• Mitochondria (drug effects, metabolism)
• Neurons (drug effects, physiology)
• Succinate Dehydrogenase (metabolism)
• Sympathectomy, Chemical
• Thyroid Gland (physiology)
• Thyroid Hormones (pharmacology)