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Energy Restriction and Starvation
Early reports that serum concentrations of T3 are reduced in states of low caloric intake (47, 49) gave rise to the concept of what we now call the Low-T3 syndrome.
Reduced T3 concentrations have been described in various conditions associated with energy deprivation, including anorexia nervosa (183–185), calorie-free diet in obesity (47), military combat training with caloric restrictions (186, 187) and other energy-deficient situations (188).
Even moderate weight loss may result in hypodeiodination with consecutive decreased T3 concentrations (189). Today, at least three mechanisms explaining this finding are known (Figure 6) (23).
In the fed state, peripheral step-up deiodination is stimulated by insulin (119) and bile acids (190–192).
In addition, increased leptin concentrations facilitate release of TRH and TSH via the hypothalamic melanocortin pathway (23, 83, 146, 193).
Together, these different mechanisms enhance conversion of T4 to T3, thus mediating postprandial thermogenesis.
Conversely, in fasting conditions concentrations of insulin, bile acids, and leptin are low, which results in decreased step-up deiodination and thyrotropic adaptation, and eventually in low-T3 syndrome.
Additional mechanisms leading to impaired TSH release include increased expression of neuromedin B, a bombesin-related peptide, which is an inhibitor of TSH secretion, and upregulation of hypothalamic D2 expression during fasting (23), resulting in low TRH expression in the PVN (25, 95, 98, 194).
https://www.frontiersin.org/articles/10.3389/fendo.2017.00163/full#F5
Early reports that serum concentrations of T3 are reduced in states of low caloric intake (47, 49) gave rise to the concept of what we now call the Low-T3 syndrome.
Reduced T3 concentrations have been described in various conditions associated with energy deprivation, including anorexia nervosa (183–185), calorie-free diet in obesity (47), military combat training with caloric restrictions (186, 187) and other energy-deficient situations (188).
Even moderate weight loss may result in hypodeiodination with consecutive decreased T3 concentrations (189). Today, at least three mechanisms explaining this finding are known (Figure 6) (23).
In the fed state, peripheral step-up deiodination is stimulated by insulin (119) and bile acids (190–192).
In addition, increased leptin concentrations facilitate release of TRH and TSH via the hypothalamic melanocortin pathway (23, 83, 146, 193).
Together, these different mechanisms enhance conversion of T4 to T3, thus mediating postprandial thermogenesis.
Conversely, in fasting conditions concentrations of insulin, bile acids, and leptin are low, which results in decreased step-up deiodination and thyrotropic adaptation, and eventually in low-T3 syndrome.
Additional mechanisms leading to impaired TSH release include increased expression of neuromedin B, a bombesin-related peptide, which is an inhibitor of TSH secretion, and upregulation of hypothalamic D2 expression during fasting (23), resulting in low TRH expression in the PVN (25, 95, 98, 194).
https://www.frontiersin.org/articles/10.3389/fendo.2017.00163/full#F5
