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Synthesis and Regulation of Thyroid Hormones01:20

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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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Functions of Thyroid Hormones01:18

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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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Glucose Homeostasis: Regulation of Blood Glucose01:02

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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
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Hormones Regulating Blood Glucose01:16

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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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Thyroid stimulating hormone increases hepatic gluconeogenesis via CRTC2.

Yujie Li1, Laicheng Wang2, Lingyan Zhou1

  • 1Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Shandong Clinical Medical Center of Endocrinology and Metabolism, Institute of Endocrinology and Metabolism, Shandong Academy of Clinical Medicine, 324 Jing 5 Rd Jinan, Shandong 250021, PR China.

Molecular and Cellular Endocrinology
|February 19, 2017
PubMed
Summary

Thyroid stimulating hormone (TSH) elevates blood glucose by activating CRTC2, a protein that enhances glucose production in the liver. This mechanism involves the TSH receptor and CREB, impacting glucose homeostasis.

Keywords:
CRTC2GluconeogenesisPEPCKTSH

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Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolism

Background:

  • Epidemiological studies link elevated thyroid stimulating hormone (TSH) to abnormal glucose levels.
  • Previous research indicated TSH directly influences gluconeogenesis, but the molecular pathways were unknown.

Purpose of the Study:

  • To elucidate the molecular mechanism by which TSH induces hepatic gluconeogenesis.
  • To investigate the role of CRTC2 (CREB-regulated transcription coactivator 2) in TSH-mediated glucose regulation.

Main Methods:

  • Utilized a mouse model of subclinical hypothyroidism with elevated TSH.
  • Employed HepG2 cells to study TSH effects on CRTC2 expression, phosphorylation, and CREB activation.
  • Assessed the impact of CRTC2 and CREB silencing on gluconeogenic gene expression (PEPCK-luciferase).
  • Examined CRTC2:CREB complex formation in mouse livers with TSH receptor (TSHR) deletion.

Main Results:

  • Subclinical hypothyroidism in mice led to increased fasting blood glucose and hepatic glucose production.
  • TSH stimulation upregulated CRTC2 expression and promoted CRTC2 dephosphorylation and p-CREB (Ser133) in HepG2 cells via the TSHR/cAMP/PKA pathway.
  • Silencing CRTC2 or CREB attenuated TSH-induced PEPCK-luciferase activity.
  • TSHR deletion in mice reduced hepatic CRTC2:CREB complex levels.

Conclusions:

  • TSH activates CRTC2 through the TSHR/cAMP/PKA signaling pathway.
  • Activated CRTC2 forms a complex with CREB, leading to increased hepatic gluconeogenesis.
  • This pathway highlights a novel mechanism linking TSH to hyperglycemia and provides potential targets for managing glucose metabolism disorders.