Triiodothyronine treatment increases substrate cycling between pyruvate carboxylase and malic enzyme in perfused rat liver

Petersen, Kitt Falk; Blair, James B.; Shulman, Gerald I.

doi:10.1016/0026-0495(95)90133-7

Cited by 28 publications

(23 citation statements)

References 12 publications

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“…However, when a regression model including randomization was used, data from [U- 13 C]lactate/[U- 13 C]pyruvate-perfused livers gave values identical to those from [U- 13 C]propionate and simple equations ( Figure 1G). Hence, in contrast to a recent report (21), but in agreement with another (22), these findings demonstrate that tracer doses of propionate do not perturb glucose production or anaplerosis and explain why [U- 13 C]pyruvate/lactate/alanine tracers provide lower estimates of pyruvate cycling when incomplete randomization is not modeled (23).…”

Section: Introductionsupporting

confidence: 57%

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

Satapati¹,

Kucejová²,

Duarte³

et al. 2015

Journal of Clinical Investigation

329

249

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Section: Introductionsupporting

confidence: 57%

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

Satapati¹,

Kucejová²,

Duarte³

et al. 2015

Journal of Clinical Investigation

329

249

View full text Add to dashboard Cite

“…However, the combination of increased IMCL content and muscle mitochondrial uncoupling we observed in RTH subjects is surprising, because in previous studies, transgenic mice with UCP3 overexpression in skeletal muscle were shown to be protected from insulin resistance due to decreased intramuscular diacylglycerol (DAG) concentrations associated with increased fat oxidation (43). One possible explanation for these discrepant results is that besides stimulating muscle fat oxidation and mitochondrial energy uncoupling in skeletal muscle, thyroid hormone also promotes myocellular lipogenesis by upregulation of malic enzyme gene expression, as has been documented in the liver (44)(45)(46). It is therefore possible that the rate of intramuscular lipogenesis exceeds the rate of oxidation, resulting in net accumulation of IMCL and DAG.…”

Section: Figurementioning

confidence: 62%

Resistance to thyroid hormone is associated with raised energy expenditure, muscle mitochondrial uncoupling, and hyperphagia

Mitchell¹,

Savage²,

Dufour³

et al. 2010

J. Clin. Invest.

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Resistance to thyroid hormone (RTH), a dominantly inherited disorder usually associated with mutations in thyroid hormone receptor β (THRB), is characterized by elevated levels of circulating thyroid hormones (including thyroxine), failure of feedback suppression of thyrotropin, and variable tissue refractoriness to thyroid hormone action. Raised energy expenditure and hyperphagia are recognized features of hyperthyroidism, but the effects of comparable hyperthyroxinemia in RTH patients are unknown. Here, we show that resting energy expenditure (REE) was substantially increased in adults and children with THRB mutations. Energy intake in RTH subjects was increased by 40%, with marked hyperphagia particularly evident in children. Rates of muscle TCA cycle flux were increased by 75% in adults with RTH, whereas rates of ATP synthesis were unchanged, as determined by 13 C/ 31 P magnetic resonance spectroscopy. Mitochondrial coupling index between ATP synthesis and mitochondrial rates of oxidation (as estimated by the ratio of ATP synthesis to TCA cycle flux) was significantly decreased in RTH patients. These data demonstrate that basal mitochondrial substrate oxidation is increased and energy production in the form of ATP synthesis is decreased in the muscle of RTH patients and that resting oxidative phosphorylation is uncoupled in this disorder. Furthermore, these observations suggest that mitochondrial uncoupling in skeletal muscle is a major contributor to increased REE in patients with RTH, due to tissue selective retention of thyroid hormone receptor α sensitivity to elevated thyroid hormone levels.

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“…[176] Thegeneration of heat is further facilitated through the induction of fultile cycles in the metabolism of glucose and fat by THs. [179] TRb-selective compounds are known to increase oxygen consumption in cholesterol-fed mice (GC-1) and rats (GC-1 and KB141). Therequired doses are higher than those required for the reduction of cholesterol, but lower than those required to produce harmful effects.…”

Section: Thyroid Hormones and Obesitymentioning

confidence: 99%

Chemistry and Biology in the Biosynthesis and Action of Thyroid Hormones

et al. 2016

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Thyroid hormones (THs) are secreted by the thyroid gland. They control lipid, carbohydrate, and protein metabolism, heart rate, neural development, as well as cardiovascular, renal, and brain functions. The thyroid gland mainly produces l-thyroxine (T4) as a prohormone, and 5'-deiodination of T4 by iodothyronine deiodinases generates the nuclear receptor binding hormone T3. In this Review, we discuss the basic aspects of the chemistry and biology as well as recent advances in the biosynthesis of THs in the thyroid gland, plasma transport, and internalization of THs in their target organs, in addition to the deiodination and various other enzyme-mediated metabolic pathways of THs. We also discuss thyroid hormone receptors and their mechanism of action to regulate gene expression, as well as various thyroid-related disorders and the available treatments.

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Triiodothyronine treatment increases substrate cycling between pyruvate carboxylase and malic enzyme in perfused rat liver

Cited by 28 publications

References 12 publications

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

Mitochondrial metabolism mediates oxidative stress and inflammation in fatty liver

Resistance to thyroid hormone is associated with raised energy expenditure, muscle mitochondrial uncoupling, and hyperphagia

Chemistry and Biology in the Biosynthesis and Action of Thyroid Hormones

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