Skip to main content
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 #68151
Title: IRON DEFICIENCY AND SUPPLEMENTATION IMPACT THERMOREGULATION AND BROWN ADIPOSE TISSUE (BAT) MITOCHONDRIAL MORPHOLOGY OF RATS EXPOSED TO COLD

Author
item Michelsen, Kim
item Hall, Clinton
item Newman Jr, Samuel
item DROKE, ELIZABETH - 5450-20-00
item Sleeper, Mary
item Lukaski, Henry

Submitted to: North Dakota Academy of Science Proceedings
Publication Type: Other
Publication Acceptance Date: 4/25/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: The role that iron (Fe) plays in regulating whole-body temperature is not well defined. Fe-deficient rats have reduced concentrations of thyroid hormones and altered body temperature. Because thyroid hormones act at the mitochondria level of brown adipose tissue to produce heat, Fe status may affect the structural characteristics of mitochondria, a cell component that produces energy to maintain body temperature. To examine the relationships among dietary iron, body temperature, thyroid hormones, and brown adipose tissue mitochondria, young male rats were fed diets containing adequate or deficient amounts of Fe. Some of the rats fed the low-Fe diets then were given the diet containing an adequate amount of Fe. When exposed to cold air for four hours, the rats fed the Fe-deficient diet had a greater decline in body temperature than the rats fed the Fe- adequate diet. The rats initially fed the Fe-deficient diet then fed the Fe-adequate diet had similar body temperatures as the animals fed the Fe- adequate diet. Plasma thyroid hormone concentrations were less in the rats fed the Fe-deficient, as compared to the Fe-adequate and Fe-deficient supplemented with adequate Fe diets. The structure of mitochondria suggests that Fe deficiency produced changes that indicate impaired heat production; this change was ameliorated with Fe supplementation. These findings indicate that Fe deficiency reduces the capability of rats to maintain body temperature during short-term cold exposure. Biological impairments of Fe deficiency lie in the production of adequate amounts of thyroid hormones and adverse changes in the mitochondria that inhibit the production of heat. This information will be useful to scientists who seek to understand how mineral elements regulate energy utilization.

Technical Abstract: As an essential element, iron (Fe) is needed for optimal function of many biological processes, including energy metabolism. Previous findings indicate that inadequate dietary iron is associated with decreased thyroid hormones in the blood. An explanation for the impaired ability to generate heat in Fe-deficiency is lacking. Structural abnormalities in the mitochondria of brown adipose tissue (BAT) may be one explanation of this impairment. A group of male, weanling, Sprague-Dawley rats was matched by weight into three dietary groups: Fe-adequate (35 ppm, FeA), Fe-deficient (7 ppm, FeD), and Fe-supplemented (FeS) (fed an FeD diet then an FeA diet). Half of the rats in each dietary group were maintained at 27 deg C and the other half were exposed to 4 deg C for 4 hours. Body temperature declined more in FeD, as compared to FeA and FeS rats. Both thyroxine and triiodothyronine were decreased at 27 deg C, and did not increase to the same degree during acute cold exposure in FeD, as compared to FeA and FeS rats. Mitochondrial morphology indicated a dominance for oxidative phosphorylation in FeD that was ameliorated with FeS toward uncoupling of oxidative phosphorylation and heat production. These findings indicate a functional impairment in energy production that may be related to hypothyroidism and altered BAT mitochondrial morphology in Fe deficiency.