The effect of L-triiodothyronine on oxidative metabolism of muscle, adipose tissue, and liver in genetically obese mice

Oh, Soomee
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Early defects before the full development of obesity in the genetically obese (ob/ob) mouse are low body oxidative metabolism and low levels of circulating thyroid hormones. I explored the possibility that early triiodothyronine (T[subscript]3) treatment may improve body oxidative metabolism by increasing oxygen consumption in metabolically important tissues such as muscle, white and brown adipose tissue, and liver in ob/ob mice. Also, the possibility was explored that early T[subscript]3 treatment of ob/ob mice will lower body fat content. Doses of T[subscript]3, ranging from 0.0 to 25.0 [mu]g/100 g body weight were injected intraperitoneally into ob/ob and nonobese (non-ob/ob) mice daily from 3 weeks until 6 weeks of age. Food intake was equalized across all groups to that consumed by the non-ob/ob saline-treated group to remove the effects of hyperphagia in ob/ob mice. At 6 weeks of age, the following parameters were analyzed: body weight, concentrations of thyroxine (T[subscript]4), T[subscript]3, thyroid stimulating hormone (TSH), insulin, and glucose in serum, body oxygen consumption, colonic temperature, body composition, and tissue oxygen consumption of muscle, white and brown adipose tissue, and liver. The treatment with T[subscript]3 decreased body weight, increased body oxygen consumption, increased colonic temperature, and decreased body fat without a significant change in body protein in ob/ob mice. This T[subscript]3 treatment also increased serum T[subscript]3, decreased serum T[subscript]4, TSH, insulin, and glucose concentrations in ob/ob mice. Because total body protein did not change as a result of T[subscript]3 treatment, the increased body oxidative metabolism due to T[subscript]3 treatment was probably via the change of metabolic activity of the lean body mass or the metabolically important tissues in ob/ob mice;The saline-treated ob/ob mice showed lower muscle weights, higher fat pad and liver weights, and larger fat cell sizes than saline-treated non-ob/ob mice. In ob/ob mice, tissue O[subscript]2 consumption was lower in muscle, white and brown adipose tissues but higher in liver as compared with saline-treated non-ob/ob mice. Early T[subscript]3 treatment in ob/ob mice during growth resulted in significantly lower values for liver weight, hepatocyte number, liver protein, epididymal fat pad weight, and white adipocyte number and size. T[subscript]3 treatment increased muscle, liver, and brown adipose tissue O[subscript]2 consumption in non-ob/ob mice. In ob/ob mice, T[subscript]3 only increased muscle O[subscript]2 consumption and required higher doses to achieve a change. These data are consistent with the concept of tissue T[subscript]3 resistance in ob/ob mice. Low T[subscript]3 levels and tissue resistance to T[subscript]3 may be important early defects in this particular obesity syndrome.

Food science and human nutrition, Nutrition