Abstract

In order to investigate the process by which dietary composition may regulate T4 conversion to T3 and reverse T3, iodothyronine levels were measured in the sera of seven obese subjects during consecutive study periods. These study periods included the ingestion of an approximate weight-maintaining diet (40% carbohydrate, 40% fat, 20% protein) during a control period of 4 days, a fast of 7 days thereafter, and then a 5-day period of glucose ingestion (50 g/day) only. The mean (±SE) serum T3 concentration was 117 ± 8 ng/dl on day 4 of the control period, and gradually decreased to 66 ± 11 ng/dl ( p < 0.01) on the last day of fasting. The subsquent administration of glucose was associated with an increase in the mean serum T3 level to 94 ± 10 ng/dl ( p < 0.01). Mean (±SE) serum levels of reverse T3 varied reciprocally and were 52 ± 9 ng/dl, 82 ± 12 ng/dl ( p < 0.005), and 65 ± 9 ng/dl (compared to fasting, p < 0.05) during the fed and fasting states and during glucose administration, respectively. Furthermore, employing a similar protocol in a different group of subjects, serum sampled during the administration of 100 g of fructose orally during days 8–12 of fasting also was associated with an increase in mean serum T3 and a decrease in mean serum reverse T3, as compared to values obtained on day 6 or day 7 of fasting (T3: 83 ± 6 ng/dl, fasting vs. 111 ± 10, fructose ( p < 0.05); rT3: 56 ± 9, fasting vs. 42 ± 6 ng/dl, fructose ( p < 0.025)). Serum T4 concentrations were not significantly altered in any study period either during glucose or fructose ingestion. Despite the decrement in serum T3 levels observed during fasting, the mean peak TSH in response to TRH stimulation in a group of 15 obese subjects was decreased during fasting as compared to the fed state (8.1 ± 1.2 μU/ml, fast vs. 12.8 ± 2.0 μU/ml, fed). These observations suggest that both glucose and fructose are capable of modulating serum T3 and reverse T3 levels and that administration of these hexoses in doses of only 100–200 g/day for 5 days may be effective in altering T4 degradative pathways. Furthermore, despite the decreased serum T3 levels, the TSH response to TRH stimulation is decreased, paradoxically, during fasting.

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