Effects of a β3-Adrenergic Agonist on Glucose Uptake and Leptin Expression and Secretion in Cultured Adipocytes from Lean and Overweight (Cafeteria) Rats

Moreno-Aliaga, María J.; Lamas, Oscar; Marti, Amelia; Martínéz, J. Alfredo

doi:10.1006/bbrc.2002.6577

Cited by 15 publications

(15 citation statements)

References 26 publications

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“…1). The overweight group (n ϭ 15) was fed a fat-rich hypercaloric "cafeteria" diet (hypercaloric diet, 467.0 kcal/100 g) composed of paté, potato chips, chocolate, bacon, biscuits, and pelleted diet in a proportion of 2:1:1:1:1:1 as previously described [11,25]. The composition was 9% of energy as protein, 29% of energy as carbohydrate and 62% of energy as lipid by dry weight (Fig.…”

Section: Animals and Dietsmentioning

confidence: 99%

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Lamas

Martínez

Marti

2004

The Journal of Nutritional Biochemistry

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Section: Animals and Dietsmentioning

confidence: 99%

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Lamas

Martínez

Marti

2004

The Journal of Nutritional Biochemistry

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“…The anti-obesity effect of ␤ 3 -AR stimulation has been well documented in various animal models of obesity, including those induced by cafeteria feeding (10,12,15,16). In this study, we also confirmed the marked fat-reducing effect of the highly selective ␤ 3 -adrenergic agonist CL in obesity induced by feeding cafeteria diets; that is, WT mice fed on cafeteria diets gained more body and WAT weights than those on laboratory chow, but a 2-wk treatment with CL completely prevented the obesity induced by cafeteria feeding.…”

mentioning

confidence: 99%

“…Such ectopic expression of UCP1 has been demonstrated in animals that were acclimated to cold environments and those treated with ␤ 3 -adrenergic agonists and/or leptin (3,10,12,(15)(16)(17)23). In contrast to UCP1, the effect of CL treatment on UCP2 and UCP3 was rather complicated; that is, UCP2 mRNA was upregulated in BAT but downregulated in WAT of UCP1-KO mice.…”

mentioning

confidence: 99%

Indispensable role of mitochondrial UCP1 for antiobesity effect of β₃-adrenergic stimulation

Inokuma

Okamatsu‐Ogura²,

Omachi³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

131

119

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. Indispensable role of mitochondrial UCP1 for antiobesity effect of ␤ 3-adrenergic stimulation. Am J Physiol Endocrinol Metab 290: E1014 -E1021, 2006. First published December 20, 2005 doi:10.1152/ajpendo.00105.2005.-Mitochondrial uncoupling protein-1 (UCP1) has been thought to be a key molecule for thermogenesis during cold exposure and spontaneous hyperphagia and thereby in the autonomic regulation of energy expenditure and adiposity. However, UCP1 knockout (KO) mice were reported to be cold intolerant but unexpectedly did not get obese even after hyperphagia, implying that UCP1 may not be involved in the regulation of adiposity. Treatment of obese animals with ␤ 3-adrenergic agonists is known to increase lipid mobilization, induce UCP1, and, finally, reduce body fat content. To obtain direct evidence for the role of UCP1 in the anti-obesity effect of ␤ 3-adrenergic stimulation, in the present study, UCP1-KO and wild-type (WT) mice were fed on cafeteria diets for 8 wk and then given a ␤ 3-adrenergic agonist, CL-316,243 (CL), or saline for 2 wk. A single injection of CL increased whole body oxygen consumption and brown fat temperature in WT mice but not in KO mice, and it elicited almost the same plasma free fatty acid response in WT and KO mice. WT and KO mice increased similarly their body and white fat pad weights on cafeteria diets compared with those on laboratory chow. Daily treatment with CL resulted in a marked reduction of white fat pad weight and the size of adipocytes in WT mice, but not in KO mice. Compared with WT mice, KO mice expressed increased levels of UCP2 in brown fat but decreased levels in white fat and comparable levels of UCP3. It was concluded that the anti-obesity effect of ␤ 3-adrenergic stimulation is largely attributable to UCP1, but less to UCP2 and UCP3, and thereby to UCP1-dependent degradation of fatty acids released from white adipose tissue.uncoupling protein-1; adiposity; CL-316,243; energy expenditure; hyperphagia UNCOUPLING PROTEIN (UCP) IS A MOLECULE, as its name suggests, that uncouples mitochondrial oxidative phosphorylation by bypassing the electrochemical gradient across the inner membrane from the F1-ATPase and thereby dissipates energy as heat. Among several isoforms of the UCP family so far reported in mammals, UCP1 is the only one whose physiological importance has been firmly established; that is, UCP1 is present exclusively in brown adipose tissue (BAT), an organ specified for nonshivering thermogenesis during cold acclimation, arousal from hibernation, and recovery from anesthetic hypothermia (2). UCP1 has also been proposed to be involved in diet-induced thermogenesis, as well as cold-induced nonshivering thermogenesis, and play a significant role in the control of energy expenditure and whole body energy balance. This is supported by the observations, for example, that spontaneous overfeeding of highly palatable diets and/or high-fat diets gives rise to increased energy expenditure (oxygen consumption) in association with BAT hyperplasia and increased UCP1 c...

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“…The improvement in glucose homeostasis induced by β3-AR agonists appears to be a consequence of increased insulin sensitivity in peripheral tissues rather than stimulation of insulin secretion by the pancreas [17]. Although, the expression of β3-AR in myocytes is still a matter of debate [18-20], obese rats treated with β3-AR agonists demonstrated an improvement of insulin sensitivity in brown and white adipose tissue as well as in skeletal muscle [17,21,22]. In adipose tissue this effect is believed to be mediated by the conversion of large adipocytes into small adipocytes, which are more sensitive to insulin [21].…”

Section: Introductionmentioning

confidence: 99%

“…The objective of the present study was to determine whether a selective β3-AR agonist could prevent alterations in the profile of skeletal muscle and adipose tissue lipids induced with the consumption of the cafeteria diet, previously reported to induce weight gain and hyperinsulinemia [22,23]. The selective β3-AR agonist ZD7114 was used in this study.…”

Section: Introductionmentioning

confidence: 99%

β3-adrenoceptor agonist prevents alterations of muscle diacylglycerol and adipose tissue phospholipids induced by a cafeteria diet

et al. 2004

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BackgroundInsulin resistance induced by a high fat diet has been associated with alterations in lipid content and composition in skeletal muscle and adipose tissue. Administration of β3-adrenoceptor (β3-AR) agonists was recently reported to prevent insulin resistance induced by a high fat diet, such as the cafeteria diet. The objective of the present study was to determine whether a selective β3-AR agonist (ZD7114) could prevent alterations of the lipid profile of skeletal muscle and adipose tissue lipids induced by a cafeteria diet.MethodsMale Sprague-Dawley rats fed a cafeteria diet were treated orally with either the β3-AR agonist ZD7114 (1 mg/kg per day) or the vehicle for 60 days. Rats fed a chow diet were used as a reference group. In addition to the determination of body weight and insulin plasma level, lipid content and fatty acid composition in gastronemius and in epididymal adipose tissue were measured by gas-liquid chromatography, at the end of the study.ResultsIn addition to higher body weights and plasma insulin concentrations, rats fed a cafeteria diet had greater triacylglycerol (TAG) and diacylglycerol (DAG) accumulation in skeletal muscle, contrary to animals fed a chow diet. As expected, ZD7114 treatment prevented the excessive weight gain and hyperinsulinemia induced by the cafeteria diet. Furthermore, in ZD7114 treated rats, intramyocellular DAG levels were lower and the proportion of polyunsaturated fatty acids, particularly arachidonic acid, in adipose tissue phospholipids was higher than in animals fed a cafeteria diet.ConclusionsThese results show that activation of the β3-AR was able to prevent lipid alterations in muscle and adipose tissue associated with insulin resistance induced by the cafeteria diet. These changes in intramyocellular DAG levels and adipose tissue PL composition may contribute to the improved insulin sensitivity associated with β3-AR activation.

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Effects of a β3-Adrenergic Agonist on Glucose Uptake and Leptin Expression and Secretion in Cultured Adipocytes from Lean and Overweight (Cafeteria) Rats

Cited by 15 publications

References 26 publications

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Indispensable role of mitochondrial UCP1 for antiobesity effect of β₃-adrenergic stimulation

β3-adrenoceptor agonist prevents alterations of muscle diacylglycerol and adipose tissue phospholipids induced by a cafeteria diet

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Effects of a β3-Adrenergic Agonist on Glucose Uptake and Leptin Expression and Secretion in Cultured Adipocytes from Lean and Overweight (Cafeteria) Rats

Cited by 15 publications

References 26 publications

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Energy restriction restores the impaired immune response in overweight (cafeteria) rats

Indispensable role of mitochondrial UCP1 for antiobesity effect of β3-adrenergic stimulation

β3-adrenoceptor agonist prevents alterations of muscle diacylglycerol and adipose tissue phospholipids induced by a cafeteria diet

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Indispensable role of mitochondrial UCP1 for antiobesity effect of β₃-adrenergic stimulation