Hyperphagia in cold-exposed rats is accompanied by  decreased plasma leptin but unchanged hypothalamic NPY

Chen, Bing; Frankish, Helen; Pickavance, Lucy; Wang, Qiong; Hopkins, David; Stock, Michael J.; Williams, Gareth

doi:10.1152/ajpregu.1998.274.1.r62

Cited by 61 publications

(71 citation statements)

References 25 publications

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“…42,43 As expected, an enhancement in BAT UCP1 mRNA levels by Trecadrine treatment was observed, as reported for other b 3 -adrenoceptor agonists such as CL 316243 and BRL 35135. 13,44 The UCP2 occurring in WAT, BAT and other tissues 38 has been reported to be differently affected by dietary intake 13,45,46 as well as other physiological and nutritional circumstances. 47,48 Thus, there are evidences about tissue-speci®c features concerning the adipose tissue and skeletal muscle in the mechanisms regulating UCP2 mRNA expression in response to fasting, refeeding or high fat intake.…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Berraondo

Marti

Duncan³

et al. 2000

Int J Obes

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OBJECTIVE: The anti-obesity properties of a new b 3 -adrenergic agonist (Trecadrine) were examined in a diet-induced obesity model, including the effects on OB and uncoupling protein (UCP-1 and -2) gene expression. MEASUREMENTS: Control rats and cafeteria-fed rats were treated with placebo or Trecadrine for 35 days. Leptin and UCP (1 and 2) mRNA levels were determined by reverse transcription ± polymerase chain reaction (RT-PCR) methodology in adipose tissue and gastrocnemius muscle. RESULTS: Animals fed a cafeteria diet increased body weight, fat content, white adipose tissue (WAT), brown adipose tissue (BAT) weights and oxygen consumption in relation to lean controls. A rise in plasma leptin, WAT OB gene expression as well as circulating free fatty acids levels was found in obese rats as compared with lean controls. Trecadrine administration to cafeteria-fed animals decreased fat content, WAT weight, circulating leptin and fatty acids concentrations, and WAT OB gene expression, reaching comparable values to lean controls, while WAT O 2 consumption was increased in these animals. Also, an increase in BAT UCP1 mRNA levels was found through a twoway analysis of variance in control and obese animals after Trecadrine administration. Gastrocnemius muscle UCP2 gene expression was reduced in lean Trecadrine-treated and diet-induced obese animals as compared to controls, while an increase was found in cafeteria-fed animals after Trecadrine administration. A negative correlation between WAT O 2 consumption and UCP2 expression was found in control animals, but not in the cafeteria-fed groups, suggesting a differential response to the b 3 -adrenergic compound in lean and obese animals, which is in agreement with the reported statistical interactions between obesity and Trecadrine administration found for WAT O 2 consumption and muscle UCP2 expression, as well as for plasma leptin and WAT leptin expression. CONCLUSION: The new b 3 -adrenergic agonist, Trecadrine, decreases fat content and increases gastrocnemius muscle UCP2 gene expression in a diet-induced obesity model. This sheds additional light on the action mechanism of compounds with af®nity for b 3 -adrenoceptors and other potential anti-obesity agents.

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Section: Discussionmentioning

confidence: 99%

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Berraondo

Marti

Duncan³

et al. 2000

Int J Obes

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“…In the wild, voles face combined stresses of lactation and cold exposure. It is well known that the development of large thermogenic capacities during cold exposure is an important mechanism to maintain body temperature in rodents (Cannon and Nedergaard, 2004), and the increase in food intake compensates for the added energy expenditure for thermogenesis (Bing et al, 1998). However, the rodents suppress thermogenic capacity in BAT (Trayhurn et al, 1982;Wade et al, 1986;Schneider and Wade, 1987;Li and Wang, 2005a) and increase food intake (Johnson et al, 2001a;Liu et al, 2003) during lactation.…”

Section: Introductionmentioning

confidence: 99%

Thermogenesis, food intake and serum leptin in cold-exposed lactating Brandt's volesLasiopodomys brandtii

Zhang

Wang

2007

Journal of Experimental Biology

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SUMMARY Lactation is the most energetically expensive period for mammals and is associated with increased metabolism and energy intake, but decreased thermogenic capacity. It is well known that small mammals increase both food intake and thermogenesis in the cold. The present study aimed to examine whether Brandt's voles Lasiopodomys brandtii could adjust energy intake and thermogenesis to accommodate simultaneous lactation and cold exposure. The voles were placed into two temperature treatments: warm(23±1°C) and cold (5±1°C). Animals at each temperature treatment were further divided into two groups: non-reproductive (NR) and lactating females. We found that lactating voles at peak lactation in the cold enhanced food intake by 2.6 g day–1 compared with those in the warm, and increased uncoupling protein 1 (UCP1) content in brown adipose tissue (BAT), to the same level as the cold-exposed NR females. Serum leptin levels decreased significantly during lactation and were positively correlated with body mass and fat mass. After correcting for the effects of body mass,residual serum leptin was negatively correlated with residual gross energy intake and residual RMR. In addition, residual serum leptin levels were positively correlated with UCP1 contents in the warm, but not in the cold. Together, these data suggest that lactating voles can increase thermogenic capacity and energy intake to meet the high energetic costs of simultaneous lactation and cold exposure. Further, serum leptin appears to be involved in the energy intake regulation and thermoregulation, but the thermoregulation in the cold may be mainly mediated by other factors.

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“…In animals acclimated to room temperature, leptin administration increased their body temperature, basal metabolic rates, nonshivering thermogenesis and UCP1 expression in IBAT, indicating a potential involvement of leptin in thermogenesis [7,11]. In contrast to this, in cold acclimated rats, leptin administration reduced IBAT thermogenesis [45], and low serum leptin levels were accompanied by an increase in UCP1 gene expression [46].…”

Section: Discussionmentioning

confidence: 80%

Leptin immunoexpression and innervation in rat interscapular brown adipose tissue of cold-acclimated rats: the effects of L-arginine and L-NAME.

Korać

Buzadžić²,

Petrović³

et al. 2008

Folia Histochem Cytobiol.

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Abstract:The aim of the present study was to explore the effect of nitric oxide on leptin immunoexpression and innervation in interscapular brown adipose tissue (IBAT) of room-and cold-acclimated rats. Animals acclimated both to roomtemperature (22 ± 1°C) and cold (4 ± 1°C) were treated with L-arginine, a substrate for nitric oxide synthases (NOSs), or N?-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOSs, for 45 days. Leptin expression and localization in brown adipocytes was studied by immunohistochemistry, and innervation stained by the Bodian method. Strong leptin immunopositivity was observed in brown adipocytes cytoplasm of all room-acclimated groups, but nuclear leptin positivity was found only in L-NAME treated rats. In cold-acclimated control and L-NAME treated rats leptin immunopositivity was absent, while L-arginine treatment reversed the cold-induced suppression of leptin expression. Comparing to control, L-arginine, and even more L-NAME, at 22 ± 1°C induced greater innervation. In conclusion, L-arginine treatment changes leptin expression pattern on cold in rat IBAT.

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Hyperphagia in cold-exposed rats is accompanied by decreased plasma leptin but unchanged hypothalamic NPY

Cited by 61 publications

References 25 publications

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Up-regulation of muscle UCP2 gene expression by a new β3-adrenoceptor agonist, trecadrine, in obese (cafeteria) rodents, but down-regulation in lean animals

Thermogenesis, food intake and serum leptin in cold-exposed lactating Brandt's volesLasiopodomys brandtii

Leptin immunoexpression and innervation in rat interscapular brown adipose tissue of cold-acclimated rats: the effects of L-arginine and L-NAME.

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