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United States Department of Agriculture

Agricultural Research Service

Title: Copper Deficiency and Supplementation Impact Thermoregulation and Brown Adipose Tissue (Bat) Mitochondrial Morphology of Rats Exposed to Cold

Authors
item Michelsen, Kim
item Hall, Clinton
item Newman Jr, Samuel
item Lukaski, Henry

Submitted to: North Dakota Academy of Science Proceedings
Publication Type: Other
Publication Acceptance Date: September 15, 1997
Publication Date: N/A

Interpretive Summary: In some mammals, the major source of heat during cold exposure is a specialized tissue called brown adipose tissue (BAT). Mitochondria in BAT are components of the cell that produce heat as well as energy. This heat production is dependent on many variables including elements such as copper, thyroid hormones and certain chemicals produced by the central nervous system. A lack in any one of these important variables results i the inability of the animal to keep warm when exposed to the cold. We compared rats fed a diet lacking in copper to others either started on a diet lacking in copper then switched to a diet with adequate copper, or maintained on a diet with adequate copper. Rats fed the low copper diet had a decrease in thyroid hormones and a greater loss of body heat when exposed to the cold. In contrast, the rats given supplemental copper after receiving the low copper diet had thyroid hormone levels and body temperatures similar to the rats fed the adequate copper diet. The shape of the inside of the mitochondria changes when there is a lack of copper in the diet. A different change occurs when the animal is exposed to the cold, even in the animals with adequate copper. Inadequate copper in the diet causes changes in the structure of BAT mitochondria that suggest an inability to produce heat. These changes imply that the copper deficient BAT cannot maintain necessary heat production because of its altered mitochondrial structure. These findings will be useful to customers who investigate how nutrients affect energy metabolism.

Technical Abstract: Non-shivering thermogenesis (NST) plays a major role in the maintenance of body temperature in mammals during acute cold exposure. One site of NST is the mitochondria of BAT; NST utilizes the uncoupling of oxidative phosphorylation to produce heat. Regulation occurs through an interaction between thyroid hormone metabolism and the sympathetic nervous system. Copper-deficient (CuD) rats have decreased circulating thyroid hormones and impaired NST when acutely exposed to cold air. The morphological changes in the mitochondria in BAT resulting from CuD is not well studied. Male weanling Sprague-Dawley rats were matched by weight and fed purified diet either maintained on an adequate in copper (CuA, >5 ppm), deficient in copper (CuD,<0.5 ppm), or started on a deficient diet then switched to an adequate diet (CuS). Thin sections of embedded BAT were used to analyze the mitochondrial ultrastructure by using a transmission electron microscope. CuD rats showed signs of deficiency: anemia, decreased ceruloplasmin and increased cholesterol concentrations. In contrast to the CuA and CuS, the CuD rats had a blunted increase in plasma T3 or T4 concentration and had a significantly more rapid decrease in total body temperature during cold exposure. Mitochondrial changes imply that CuD rats at room temperature rely to a greater extent on oxidative phosphorylation for ATP production than do CuA or CuS rats. Also, the shift away from oxidative phosphorylation during cold exposure in CuD rats is significantly greater than in CuA or CuS rats. Short-term supplementation of CuD rats with Cu ameliorates the anemia, reduced ceruloplasmin concentration and hypercholesteremia. Supplementation also restored thyroid hormone and lipid status needed to promote NST.

Last Modified: 7/24/2014
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