Increased insulin binding and glucose transport in white adipocytes isolated from C57B16obob mice treated with the thermogenic β-adrenoceptor agonist BRL 26830

Young, Paul; King, Laura B.; Cawthorne, Michael A.

doi:10.1016/0006-291x(85)90928-3

Cited by 15 publications

(4 citation statements)

References 17 publications

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“…These results are also consistent with those of previous studies with BRL 26830A in db/db mice (3) and yellow KK mice (19). Acute administration of BRL 26830A increases insulin secretion from the pancreas (18,21,22), whereas chronic administration of the drug enhances tissue sensitivity to insulin by, for example, increasing the number of insulin receptors (19,23,24). The CL 316,243-induced improvement in hyper¬ glycémie in the present study therefore may be attributable to an increased tissue sensitivity to insulin that results from a decrease in body mass.…”

Section: Discussionsupporting

confidence: 92%

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

Yoshida

Sakane²,

Wakabayashi³

et al. 1994

European Journal of Endocrinology

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The effects of CL 316,243, a highly specific beta 3-adrenoceptor agonist (relative selectivities of 0, 1 and 100,000 for beta 1-, beta 2- and beta 3-receptors, respectively), were evaluated in mice with monosodium L-glutamate (MSG)-induced obesity as well as in control mice injected with physiological saline instead of MSG. Both MSG- and saline-treated mice were divided into three groups and at 8 weeks of age received either CL 316,243 (0.1 or 1.0 mg/kg) or distilled water through a gastric tube for 2 weeks. CL 316,243 not only reduced white adipose tissue mass but also activated brown adipose tissue and systemic metabolism, and hence reduced body mass without affecting food intake. Furthermore, CL 316,243 decreased hyperglycemia and hypertriglyceridemia in MSG-treated mice. However, at the higher dose, CL 316,243 also increased liver triglyceride in MSG-treated mice. These observations suggest that CL 316,243 exerts an anti-obesity effect in mice with MSG-induced obesity and consequently may prove efficacious in the treatment of human obesity.

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Section: Discussionsupporting

confidence: 92%

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

Yoshida

Sakane²,

Wakabayashi³

et al. 1994

European Journal of Endocrinology

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“…However, several studies have found that acute administration of a β 3 ‐adrenergic agonist in different animal models stimulates glucose uptake and utilization in peripheral tissues[10]. Nevertheless, results are controversial concerning glucose uptake in BAT, WAT, heart and skeletal muscle after the in‐vivo administration of a β 3 ‐adrenergic agonist[10, 17, 34]. In this sense, in‐vitro studies are appropriate to avoid the interaction of hormones.…”

Section: Discussionmentioning

confidence: 99%

A b₃‐adrenergic agonist increases muscle GLUT1/GLUT4 ratio, and regulates liver glucose utilization in diabetic rats*

Milagro¹,

Gómez-Ambrosi²,

Forga³

et al. 1999

Diabetes Obesity Metabolism

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Trecadrine reduces glucose output from the liver, thus thus contributing to the reduction of plasma glucose levels to achieve the values of control rats. Furthermore, Trecadrine administration stimulates glucose uptake in skeletal muscle, especially in those muscles with predominant glycolytic fast-twitched fibres, apparently by a direct non-insulin-dependent mechanism, involving a relative increase in the content of GLUT1 in the plasma membrane as compared with GLUT4. In conclusion, Trecadrine shows a potent hypoglycaemic effect in the alloxan-induced model of diabetes in rats by decreasing hepatic glucose output and improving muscle glucose uptake.

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“…Chronic dosing of obese animals with selective β 3 ‐AR agonists has been reported to improve glucose tolerance over 14 days (Wilbraham et al ., 1994; Young et al ., 1985) and to normalize plasma glucose levels over 14–28 days (Arbeeny et al ., 1995; Wilbraham et al ., 1994; Ghorbani & Himms‐Hagen, 1997). Chronic dosing with SR 58611A confirmed these findings.…”

Section: Discusisonmentioning

confidence: 99%

“…Fourteen day administration of selective β 3 ‐AR agonists has previously been reported to increase white adipocyte insulin binding and receptor number in lean and obese diabetic mice (Yoshida et al ., 1994; Young et al ., 1985), both actions which would tend to improve insulin sensitivity. Such chronically induced changes are unlikely to explain the positive effect of acute SR 58611A on the sensitivity to insulin.…”

Section: Discusisonmentioning

confidence: 99%

Sustained improvement in glucose homeostasis in lean and obese mice following chronic administration of the β₃ agonist SR 58611A

Williams

Shih

Taberner

1999

British J Pharmacology

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1 Acute SR 58611A (0.25 mg kg 71 ), was eective in reducing the blood glucose response to a glucose tolerance test (GTT) in normal lean (control) and spontaneously obese/diabetic CBA/Ca mice and to be equipotent to 1.25 mg kg 71 glibenclamide in lean mice. 2 Neither brown (BAT) nor white (WAT) adipose tissue lipogenesis was altered by acute SR 58611A (2 ± 8 mg kg 71 ) in lean mice, but both increased signi®cantly at the higher doses in the obese mice. 3 Acute SR 58611A produced a hypoglycaemia 40 min after dosing in lean and obese animals, the duration and potency of which was less than that of glibenclamide. Plasma insulin levels increased 20 min after acute SR 58611A and glibenclamide in lean and obese mice. 4 Chronic treatment (0.25 mg kg 71 , 15 days) with SR 58611A increased its eectiveness in improving glucose tolerance, but did not aect the body weight (BW) or food intake of either lean or obese mice. 5 Acute and chronic SR 58611A prolonged the hypoglycaemic eect of exogenous insulin in lean but not obese mice. 6 In fed and fasted lean mice and in fasted obese mice chronic SR 58611A produced an acute hypoglycaemia 30 min post administration which was greater than after a single dose. 7 SR 58611A maintained its eectiveness in improving glucose tolerance in lean and obese mice over a dosing period of 15 days. The improvement in glucose tolerance was achieved at a dose less than that required to stimulate adipose tissue lipogenesis and which did not aect food intake or body weight.

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Increased insulin binding and glucose transport in white adipocytes isolated from C57B16obob mice treated with the thermogenic β-adrenoceptor agonist BRL 26830

Cited by 15 publications

References 17 publications

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

A b₃‐adrenergic agonist increases muscle GLUT1/GLUT4 ratio, and regulates liver glucose utilization in diabetic rats*

Sustained improvement in glucose homeostasis in lean and obese mice following chronic administration of the β₃ agonist SR 58611A

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Increased insulin binding and glucose transport in white adipocytes isolated from C57B16obob mice treated with the thermogenic β-adrenoceptor agonist BRL 26830

Cited by 15 publications

References 17 publications

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

Anti-obesity effect of CL 316,243, a highly specific β3-adrenoceptor agonist, in mice with monosodium-l-glutamate-induced obesity

A b3‐adrenergic agonist increases muscle GLUT1/GLUT4 ratio, and regulates liver glucose utilization in diabetic rats*

Sustained improvement in glucose homeostasis in lean and obese mice following chronic administration of the β3 agonist SR 58611A

Contact Info

Product

Resources

About

A b₃‐adrenergic agonist increases muscle GLUT1/GLUT4 ratio, and regulates liver glucose utilization in diabetic rats*

Sustained improvement in glucose homeostasis in lean and obese mice following chronic administration of the β₃ agonist SR 58611A