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Gen Comp Endocrinol. 2017 Oct 1;252:36-47. doi: 10.1016/j.ygcen.2017.07.023. Epub 2017 Jul 22.

Increased sensitivity of thyroid hormone-mediated signaling despite prolonged fasting.

Author information

1
Department of Molecular and Cellular Biology, University of California Merced, 5200 North Lake Road, Merced, CA 95343, USA. Electronic address: bmartinez26@ucmerced.edu.
2
Department of Physics, University of California Merced, 5200 North Lake Road, Merced, CA 95343, USA.
3
Departamento de Ciencias Químico Biológicas y Agropecuarias, Universidad de Sonora, Lázaro Cárdenas del Río No. 100, Francisco Villa, Navojoa, Sonora 85880, Mexico.
4
Texas A&M Veterinary Diagnostic Laboratory, 1 Sippel Road, College Station, TX 77843, USA.
5
Department of Biology, Sonoma State University, 1801 E. Cotati Avenue, Rohnert Park, CA 94928, USA.
6
Department of Molecular and Cellular Biology, University of California Merced, 5200 North Lake Road, Merced, CA 95343, USA.

Abstract

Thyroid hormones (TH) can increase cellular metabolism. Food deprivation in mammals is typically associated with reduced thyroid gland responsiveness, in an effort to suppress cellular metabolism and abate starvation. However, in prolonged-fasted, elephant seal pups, cellular TH-mediated proteins are up-regulated and TH levels are maintained with fasting duration. The function and contribution of the thyroid gland to this apparent paradox is unknown and physiologically perplexing. Here we show that the thyroid gland remains responsive during prolonged food deprivation, and that its function and production of TH increase with fasting duration in elephant seals. We discovered that our modeled plasma TH data in response to exogenous thyroid stimulating hormone predicted cellular signaling, which was corroborated independently by the enzyme expression data. The data suggest that the regulation and function of the thyroid gland in the northern elephant seal is atypical for a fasted animal, and can be better described as, "adaptive fasting". Furthermore, the modeling data help substantiate the in vivo responses measured, providing unique insight on hormone clearance, production rates, and thyroid gland responsiveness. Because these unique endocrine responses occur simultaneously with a nearly strict reliance on the oxidation of lipid, these findings provide an intriguing model to better understand the TH-mediated reliance on lipid metabolism that is not otherwise present in morbidly obese humans. When coupled with cellular, tissue-specific responses, these data provide a more integrated assessment of thyroidal status that can be extrapolated for many fasting/food deprived mammals.

KEYWORDS:

Deiodinase; Fasting; Mathematical modeling; Obesity; Thyroid hormone receptor; Thyroid hormones; Thyroid stimulating hormone; Thyroxine

PMID:
28743556
PMCID:
PMC5580341
DOI:
10.1016/j.ygcen.2017.07.023
[Indexed for MEDLINE]
Free PMC Article

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