Differential Regulation of Mouse Uncoupling Proteins among Brown Adipose Tissue, White Adipose Tissue, and Skeletal Muscle in Chronic β3Adrenergic Receptor Agonist Treatment

Yoshitomi, Hideki; Yamazaki, Kazuto; Abe, Shinya; Tanaka, Isao

doi:10.1006/bbrc.1998.9746

Cited by 68 publications

(44 citation statements)

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“…47 The effects of b 3 -adrenergic agonists on UCP2 gene expression, which seems also to be tissue-dependent, have been reported inconsistently by investigators. Thus, an increase in WAT and BAT UCP2 gene expression after b 3 -adrenergic agonist administration has been found, 40,49 while the UCP2 expression was strikingly decreased in skeletal muscle after adrenergic agonist administration in lean animals, 52 but not in Zucker rats. 53 In our study, control rats treated with Trecadrine had reduced muscle UCP2 expression, which could be related to changes in plasma insulin and free fatty acids (FFA), since it has been reported that the levels of insulin and FFA may be important regulators of the muscle UCP2 expression.…”

Section: Discussionmentioning

confidence: 85%

“…53 In our study, control rats treated with Trecadrine had reduced muscle UCP2 expression, which could be related to changes in plasma insulin and free fatty acids (FFA), since it has been reported that the levels of insulin and FFA may be important regulators of the muscle UCP2 expression. 52 On the contrary, Trecadrine treatment enhanced gastrocnemius muscle UCP2 mRNA levels in obese animals. In this context, it is remarkable that cold, as well as T 3 administration appears to up-regulate UCP2 gene expression, 49 which was accompanied by lower body weights in the T 3 -treated animals.…”

Section: Discussionmentioning

confidence: 99%

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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: 85%

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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“…It is well known that BAT is richly innervated by sympathetic nerves (6). Expression of UCP-1 and UCP-3 in BAT and WAT is known to be modulated, in part, by ␤ 3 agonists, indicating sympathetic influence on UCP expression (44). According to previous studies, hypothalamic neuronal histamine affects peripheral lipid metabolism and autonomic function (38,41).…”

Section: Discussionmentioning

confidence: 97%

Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

et al. 2001

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Leptin resistance has recently been confirmed not only in animal obese models but in human obesity. Evidence is rapidly emerging that suggests that activation of histamine signaling in the hypothalamus may have substantial anti-obesity and antidiabetic actions, particularly in leptin-resistant states. To address this issue, effects of central, chronic treatment with histamine on food intake, adiposity, and energy expenditure were examined using leptin-resistant obese and diabetic mice. Infusion of histamine (0.05 µmol · g body wt -1 · day -1 ) into the lateral cerebroventricle (i.c.v.) for 7 successive days reduced food intake and body weight significantly in both diet-induced obesity (DIO) and db/db mice. Histamine treatment reduced body fat weight, ob gene expression, and serum leptin concentration more in the model mice than in pair-fed controls. O besity, a common metabolic disorder characterized by chronic imbalance in energy intake and energy expenditure, is a serious risk factor for type 2 diabetes, coronary artery disease, hypertension, hyperlipidemia, and other common diseases (1). The pathophysiological basis of obesity, however, is poorly understood. Since discovery of the ob gene and its encoded protein leptin (2), it has been understood that leptin acts as a hormone at the level of the hypothalamus to inhibit food intake and favor energy expenditure (3-5). The uncoupling protein (UCP) family, consisting of inner mitochondrial proteins (6-9), is known to contribute to improvement of energy imbalance resulting from energy insufficiency or excess (7,10). Gene expression of the UCP family is highly responsive to neural and humoral factors (10-14), particularly leptin (14). Serum leptin thus reflects energy stores in adipose tissue and serves to signal the brain (15). To improve understanding of the leptin signaling pathway, a number of approaches have been tried to clarify the roles of leptin-modulated hypothalamic neuropeptides in the regulation of feeding behavior and energy homeostasis (16-18).Leptin negatively regulates orexigenic neuropeptide Y (16) and agouti gene-related protein (17) and positively regulates anorexigenic proopio-melanocortin-derived peptide through leptin receptors on neurons in the hypothalamic arcuate nucleus (18). Anorexigenic corticotropin-releasing hormone in the paraventricular nucleus, which negatively affects neuropeptide Y neurons in the arcuate nucleus (19), is also positively regulated by leptin (20). The signals from such sites in the mediobasal hypothalamus thus communicate the neural underpinning of hunger and satiety with the orexigenic mediators orexin (21) and melanocortin concentrating hormone (22), both of which originate in the lateral hypothalamus.Serum concentration of leptin is known to be increased in the great majority of obese humans as well as in most rodent models, indicating that most obesity is leptin resistant (23,24). Although the details and molecular basis of the mechanisms are unknown, important factors are indicated by the following findings. F...

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“…The hypothalamo-pituitary-thyroid axis and activation of uncoupling protein-1 by way of sympathetic nervous system stimulation are known to influence thermogenesis and basal metabolic rate. 68,69 The PVH, which is associated with the regulation of food ingestion and contains numerous thyrotropin-releasing-hormone-containing neurons, 70 acts as the central hypothalamic regulator of the hypothalamo-pituitarythyroid axis. Similar to other orexigenic peptides such as NPY 71 and agouti-related protein, 72 administration of GALP into the PVH decreases the level of plasma thyroid-simulating hormone within 10 min.…”

Section: Anorexigenic Effect Of Galp On Feeding Behavior and Energy Mmentioning

confidence: 99%

Galanin-like peptide: a key player in the homeostatic regulation of feeding and energy metabolism?

et al. 2010

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The hypothalamus has a critical role in the regulation of feeding behavior, energy metabolism and reproduction. Galanin-like peptide (GALP), a novel 60 amino-acid peptide with a nonamidated C-terminus, was first discovered in porcine hypothalamus. GALP is mainly produced in the hypothalamic arcuate nucleus and is involved in the regulation of feeding behavior and energy metabolism, with GALP-containing neurons forming networks with several feeding-regulating peptide-containing neurons. The effects of GALP on food intake and body weight are complex. In rats, the central effect of GALP is to first stimulate and then reduce food intake, whereas in mice, GALP has an anorectic function. Furthermore, GALP regulates plasma luteinizing hormone levels through activation of gonadotropin-releasing hormone-producing neurons, suggesting that it is also involved in the reproductive system. This review summarizes the research on these topics and discusses current evidence regarding the function of GALP, particularly in relation to feeding and energy metabolism. We also discuss the effects of GALP activity on food intake, body weight and locomotor activity after intranasal infusion, a clinically viable mode of delivery.

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Differential Regulation of Mouse Uncoupling Proteins among Brown Adipose Tissue, White Adipose Tissue, and Skeletal Muscle in Chronic β3Adrenergic Receptor Agonist Treatment

Cited by 68 publications

References 0 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

Central Infusion of Histamine Reduces Fat Accumulation and Upregulates UCP Family in Leptin-Resistant Obese Mice

Galanin-like peptide: a key player in the homeostatic regulation of feeding and energy metabolism?

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