Regulation of brown adipose tissue lipogenesis by thyroid hormone and the sympathetic nervous system

Yeh, Wen-Ji; Leahy, Patrick; Freake, Hedley C.

doi:10.1152/ajpendo.1993.265.2.e252

Cited by 10 publications

(12 citation statements)

References 25 publications

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“…Northern analysis. Total RNA was size-separated by electrophoresis in a 1% agarose gel with formaldehyde as reported by Yeh et al (22). RNA was then transferred overnight to a nitrocellulose membrane (0.45 mm; MSI NitroPure, Westborough, MA) by the Northern procedure, using 20× standard saline citrate (SSC) buffer (1 × SSC = 150 mM NaCl, 15 mM Na citrate).…”

Section: Methodsmentioning

confidence: 99%

Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl‐CoA reductase activity and mRNA abundance in the guinea pig

Conde¹,

Roy²,

Freake³

et al. 1999

Lipids

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The effects of atorvastatin and simvastatin on hydroxy methylglutaryl (HMG)-CoA reductase activity and mRNA abundance were studied in guinea pigs randomized to three groups: untreated animals and those treated with 20 mg/kg of atorvastatin or simvastatin. Guinea pigs were fasted for 0, 6, 12, or 18 h in an attempt to remove the drug from their systems. Reductase activity and mRNA levels were analyzed after each time point. Reductase inhibitor treatment resulted in 50-62% lower cholesterol concentrations compared to untreated guinea pigs (P < 0.0001), while plasma triacylglycerol (TAG) concentrations did not differ among groups. Plasma cholesterol and TAG were 50-70% lower after 18 h fasting in the three groups (P < 0.001). In the nonfasting state, simvastatin and atorvastatin treatment did not affect HMG-CoA reductase activity compared with untreated animals. However, after 6 h of fasting, simvastatin-treated guinea pigs had higher HMG-CoA reductase activity than untreated animals (P < 0.01), suggesting that the drug had been removed from the enzyme. In contrast, atorvastatin-treated guinea pigs maintained low enzyme activity even after 18 h of fasting. Further, HMG-CoA reductase mRNA abundance was increased by sevenfold after atorvastatin treatment and by twofold after simvastatin treatment (P < 0.01). These results suggest that simvastatin and atorvastatin have different half-lives, which may affect HMG-CoA reductase mRNA levels. The increase in reductase activity by simvastatin during fasting could be related to an effect of this statin in stabilizing the enzyme. In contrast, atorvastatin, possibly due to its longer half-life, prolonged inhibition of HMG-CoA reductase activity and resulted in a greater increase in mRNA synthesis.

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Section: Methodsmentioning

confidence: 99%

Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl‐CoA reductase activity and mRNA abundance in the guinea pig

Conde¹,

Roy²,

Freake³

et al. 1999

Lipids

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“…TH increases lipogenesis in rats [71], as it directly stimulates transcription of lipogenic enzymes [72][73][74]. Of note, Yeh et al show that T 3 rescues lipogenesis as well as expression of Acc and Fas messenger RNAs (mRNAs) in the denervated BAT in hypothyroid rats [75]. In fact, T 3 has been routinely added in the differentiation cocktail for brown adipocytes due to its direct and supportive roles in adipogenesis.…”

Section: Th Increases Lipogenesismentioning

confidence: 99%

Thermogenesis in Adipose Tissue Activated by Thyroid Hormone

Yau

Yen

2020

IJMS

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Thermogenesis is the production of heat that occurs in all warm-blooded animals. During cold exposure, there is obligatory thermogenesis derived from body metabolism as well as adaptive thermogenesis through shivering and non-shivering mechanisms. The latter mainly occurs in brown adipose tissue (BAT) and muscle; however, white adipose tissue (WAT) also can undergo browning via adrenergic stimulation to acquire thermogenic potential. Thyroid hormone (TH) also exerts profound effects on thermoregulation, as decreased body temperature and increased body temperature occur during hypothyroidism and hyperthyroidism, respectively. We have termed the TH-mediated thermogenesis under thermoneutral conditions “activated” thermogenesis. TH acts on the brown and/or white adipose tissues to induce uncoupled respiration through the induction of the uncoupling protein (Ucp1) to generate heat. TH acts centrally to activate the BAT and browning through the sympathetic nervous system. However, recent studies also show that TH acts peripherally on the BAT to directly stimulate Ucp1 expression and thermogenesis through an autophagy-dependent mechanism. Additionally, THs can exert Ucp1-independent effects on thermogenesis, most likely through activation of exothermic metabolic pathways. This review summarizes thermogenic effects of THs on adipose tissues.

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“…NA treatment. Yeh et al (33) obtained indirect evidences of the T 3 effect on UCP expression in vivo, where T 3 treatment of denervated BAT produced an increment in UCP expression. Cassard-Doulcier et al (34) identified a domain in the UCP gene promoter containing a directly repeated sequence that was able to bind retinoic X and triiodothyronine receptors.…”

Section: Table I Effect Of T 3 On [ 3 H]gdp-binding Capacity To Mitocmentioning

confidence: 99%

Triiodothyronine Induces the Transcription of the Uncoupling Protein Gene and Stabilizes Its mRNA in Fetal Rat Brown Adipocyte Primary Cultures

Guerra¹,

Roncero

Porrás

et al. 1996

Journal of Biological Chemistry

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Confluent fetal rat brown adipocytes in primary culture showed an almost undetectable level of uncoupling protein (UCP) mRNA and a low mitochondrial content of functional UCP. Treatment of confluent cells with 10 nM triiodothyronine in a serum-free medium, in the absence of noradrenergic stimulation, increased the amount of UCP mRNA in a time-dependent manner. This effect was due to an increased UCP gene transcription rate and UCP mRNA stabilization, resulting in a higher content of immunoreactive mitochondrial UCP and functional UCP (detected by its ability to bind GDP). Thus, triiodothyronine might play a significant physiological role in the UCP expression throughout fetal development, when brown adipose tissue starts to differentiate and UCP is primarily expressed.

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Regulation of brown adipose tissue lipogenesis by thyroid hormone and the sympathetic nervous system

Cited by 10 publications

References 25 publications

Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl‐CoA reductase activity and mRNA abundance in the guinea pig

Atorvastatin and simvastatin have distinct effects on hydroxy methylglutaryl‐CoA reductase activity and mRNA abundance in the guinea pig

Thermogenesis in Adipose Tissue Activated by Thyroid Hormone

Triiodothyronine Induces the Transcription of the Uncoupling Protein Gene and Stabilizes Its mRNA in Fetal Rat Brown Adipocyte Primary Cultures

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