Acute cold-induced suppression of <i>ob</i> (obese) gene expression in white adipose tissue of mice: mediation by the sympathetic system

Trayhurn, Paul; Duncan, Jackie; Rayner, D V

doi:10.1042/bj3110729

Cited by 306 publications

(257 citation statements)

References 20 publications

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“…It is established that catecholamines suppress leptin production from adipose tissue in animals, 1 and we previously con®rmed this ®nding in humans with isoprenaline. 2 In vivo, sympathetic nervous system (SNS) responses are regulated by TH, and it is also established that thyroid disease alters b-adrenoceptor sensitivity in adipocytes, 3 rather than NA secretion.…”

Section: Introductionsupporting

confidence: 57%

Thyroid and sympathetic influences on plasma leptin in hypothyroidism and hyperthyroidism

et al. 2000

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Objectives: To determine the dependence of plasma leptin concentrations upon circulating noradrenaline (NA) and thyroid hormones (TH) in humans. Design: Cross-sectional study in 40 newly diagnosed untreated patients with primary thyroid disease, and 69 lean and obese euthyroid control subjects. Measurements: Plasma leptin, NA, free T3 (fT3) and TSH in the fasting state. Anthropometry and % body fat (electrical bioimpedance). Results: Leptin levels were highest in 37 obese euthyroid and 22 hypothyroid (median [interquartiles]31.5 [19.0 ± 48.0], 19.2 [11.5 ± 31.5] ng ml 71 ), and lowest in 32 lean euthyroid and 18 hyperthyroid subjects (6.6 [3.9 ± 14.4], 8.9 [5.5 ± 11.1]; ANOVA, P`0.0001). Plasma NA was similar in all groups (P n.s.). In obese controls, TSH correlated with % body fat and leptin (r 0.67, r 0.61; P`0.001). Treatment of hypothyroidism (n 10) with T4 reduced leptin from 20. 8 [11.8 ± 31.6] to 12.9 [4.6 ± 21.2] (P 0.005) with no change in BMI. Conclusions: Thyroid status modi®es leptin secretion independently of adiposity and NA. The data suggest leptin ± thyroid interactions at hypothalamic and adipocyte level.

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Section: Introductionsupporting

confidence: 57%

Thyroid and sympathetic influences on plasma leptin in hypothyroidism and hyperthyroidism

et al. 2000

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“…The membranes were prehybridized in Easyhyb solution (Boehringer Mannheim) at 428C for 1 h and hybridized in the same solution with a digoxigeninlabelled 32-mer antisense oligonucleotide probe for mouse UCP-1 (Trayhurn and Duncan, 1994), or digoxigenin-labelled 30-mer oligonucleotide probes for mouse UCP-2 and -3 . Each blot was stripped and re-probed for 18S rRNA with a 31-mer digoxigenin-labelled oligonucleotide, as previously described (Trayhurn et al, 1995). Autoradiographs were quantitated by densitometry with image-analysis (AIS System, Imaging Technology, Brock University, St Catharine's, Ontario, Canada).…”

Section: Northern Blottingmentioning

confidence: 99%

Expression of uncoupling proteins-1, -2 and -3 mRNA is induced by an adenocarcinoma-derived lipid-mobilizing factor

et al. 2002

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The abnormalities of lipid metabolism observed in cancer cachexia may be induced by a lipid-mobilizing factor produced by adenocarcinomas. The specific molecules and metabolic pathways that mediate the actions of lipid-mobilizing factor are not known. The mitochondrial uncoupling proteins-1, -2 and -3 are suggested to play essential roles in energy dissipation and disposal of excess lipid. Here, we studied the effects of lipid-mobilizing factor on the expression of uncoupling proteins-1, -2 and -3 in normal mice. Lipid-mobilizing factor isolated from the urine of cancer patients was injected intravenously into mice over a 52-h period, while vehicle was similarly given to controls. Lipid-mobilizing factor caused significant reductions in body weight (710%, P=0.03) and fat mass (720%, P50.01) accompanied by a marked decrease in plasma leptin (759%, P50.01) and heavy lipid deposition in the liver. In brown adipose tissue, uncoupling protein-1 mRNA levels were elevated in lipid-mobilizing factor-treated mice (+96%, P50.01), as were uncoupling proteins-2 and -3 (+57% and +37%, both P50.05). Lipid-mobilizing factor increased uncoupling protein-2 mRNA in both skeletal muscle (+146%, P50.05) and liver (+142%, P=0.03). The protein levels of uncoupling protein-1 in brown adipose tissue and uncoupling protein-2 in liver were also increased with lipid-mobilizing factor administration (+49% and +67%, both P=0.02). Upregulation by lipid-mobilizing factor of uncoupling proteins-1, -2 and -3 in brown adipose tissue, and of uncoupling protein-2 in skeletal muscle and liver, suggests that these uncoupling proteins may serve to utilize excess lipid mobilized during fat catabolism in cancer cachexia.

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“…To check the loading and transfer of RNA during blotting, the blot was stripped and re-probed for 18S rRNA with a 31-mer digoxigenin-labelled antisense oligonucleotide at a concentration of 10 pg ml 71 , as previously described (Trayhurn et al, 1995). The amount of NPY mRNA was expressed as the NPY mRNA/18S rRNA ratio.…”

Section: Measurements Of Npy Mrnamentioning

confidence: 99%

“…UCP-1 mRNA measurements employed a digoxigenin-labelled 32-mer antisense oligonucleotide (Trayhurn & Duncan, 1994), and ob mRNA a 33-mer antisense oligonucleotide (Trayhurn et al, 1995). 18S rRNA levels were similarly determined as a reference for both UCP-1 mRNA and ob gene, and mRNA levels were expressed as the ratio of UCP-1/18S or ob/18S signals.…”

Section: Measurements Of Ucp-1 Mrna and Ob Mrnamentioning

confidence: 99%

The effect of moxonidine on feeding and body fat in obese Zucker rats: role of hypothalamic NPY neurones

Chen

King

Pickavance

et al. 1999

British J Pharmacology

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1 The antihypertensive agent moxonidine, an imidazoline I i -receptor agonist, also induces hypophagia and lowers body weight in the obese spontaneously hypertensive rat, but the central mediation of this action and the neuronal pathways that moxonidine may interact with are not known. We studied whether moxonidine has anti-obesity e ects in the genetically-obese and insulinresistant fa/fa Zucker rat, and whether these are mediated through inhibition of the hypothalamic neuropeptide Y (NPY) neurones. 2 Lean and obese Zucker rats were given moxonidine (3 mg kg 71 day 71 ) or saline by gavage for 21 days. 3 Moxonidine decreased food intake throughout by 20% in obese rats (P50.001) and by 8% in lean rats (P50.001), and reduced weight gain that ®nal body weight was 15% lower in obese (P50.001) and 7% lower in lean (P50.01) rats than their untreated controls. Plasma insulin and leptin levels were decreased in moxonidine-treated obese rats (P50.01 and P50.05), but unchanged in treated lean rats. Uncoupling protein-1 gene expression in brown adipose tissue was stimulated by 40 ± 50% (P40.05) in both obese and lean animals given moxonidine. Obese animals given moxonidine showed a 37% reduction in hypothalamic NPY mRNA levels (P=0.01), together with signi®cantly increased NPY concentrations in the paraventricular nucleus (P50.05), but no changes in the arcuate nucleus or other nuclei; this is consistent with reduced NPY synthesis in the arcuate nucleus and blocked release of NPY in the paraventricular nucleus. In lean animals, moxonidine did not a ect NPY levels or NPY mRNA. 4 The hypophagic, thermogenic and anti-obesity e ects of moxonidine in obese Zucker rats may be partly due to inhibition of the NPY neurones, whose inappropriate overactivity may underlie obesity in this model.

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Acute cold-induced suppression of ob (obese) gene expression in white adipose tissue of mice: mediation by the sympathetic system

Cited by 306 publications

References 20 publications

Thyroid and sympathetic influences on plasma leptin in hypothyroidism and hyperthyroidism

Thyroid and sympathetic influences on plasma leptin in hypothyroidism and hyperthyroidism

Expression of uncoupling proteins-1, -2 and -3 mRNA is induced by an adenocarcinoma-derived lipid-mobilizing factor

The effect of moxonidine on feeding and body fat in obese Zucker rats: role of hypothalamic NPY neurones

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