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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #65579

Title: IMPROVED THERMOREGULATION OF COPPER-DEFICIENT (CUD) RATS IN THE COLD IS THERESULT OF ALTERED THYROID AND CATECHOLAMINE METABOLISM

Author
item Lukaski, Henry
item Hall, Clinton
item Michelsen, Kim
item Sleeper, Mary

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 4/14/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: CuD rats maintained at thermoneutral temperatures have altered metabolism of thyroid hormones and catecholamines which are needed for increased heat production in the cold. Weanling male Sprague-Dawley rats (n=42) matched by weight were fed diets adequate in Cu (CuA, 6 ppm Cu), CuD (0.6 ppm Cu) for 5 wk, or supplemented with Cu (CuS, 6 ppm Cu) for 4 d after receiving CuD for 31 d. Rats from each group (n=7) were either kept at 27 deg C or placed in cold air (4 deg C) for 8 h. CuS increased (p<0.01) hemoglobin (120 vs 86 g/L) and ceruplasmin (33 vs 5 mg/dL) as compared to CuD, but was less (p<0.05) than CuA values (150 g/L and 58 mg/dL). Body temperature in the cold declined more (p<0.002) in CuD than CuA and CuS (- 0.267 vs -0.003 and -0.019 deg C/h). Plasma T**4 and T**3 concentrations were reduced (p<0.003) in CuD as compared to CuA; values in CuS were similar to CuA. Liver and BAT deiodinase activities were decreased (p<0.01) in CuD relative to CuA and CuS. In BAT, norepinephrine (NE) was decreased (1.4 vs 2.8 and 2.2 ng/mg; p<0.01) and dopamine (DA) was increased (1.4 vs 0.17 and 0.21 ng/mg; p<0.01) in CuD as compared to CuA and CuS. These changes in NE and DA content in BAT are consistent with reduced activity of dopamine-beta-monooxygenase, a Cu-dependent enzyme. Thus, CuD impacts thermoregulatory function by decreasing production of NE in BAT which limits the conversion of T**4 to T**3 during acute cold exposure.