Involvement of β3-adrenergic receptors in the control of food intake in rats

Kanzler, Sandro Aparecido; Januário, Ana Cláudia; Paschoalini, Marta Aparecida

doi:10.1590/s0100-879x2011007500127

Cited by 17 publications

(11 citation statements)

References 36 publications

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“…effect accompanied by an increase in the latency to start eating. Similar result was obtained in a previous study after administration of beta 3 adrenergic receptor agonist [16].…”

Section: Discussionsupporting

confidence: 91%

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Hajinezhad¹,

Shohreh²

2016

Zahedan J Res Med Sci

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“…effect accompanied by an increase in the latency to start eating. Similar result was obtained in a previous study after administration of beta 3 adrenergic receptor agonist [16].…”

Section: Discussionsupporting

confidence: 91%

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Hajinezhad¹,

Shohreh²

2016

Zahedan J Res Med Sci

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“…administration of propranolol (50ug/day), ICI-118,551 (30ug/day), SR59230A (20ug/day), or vehicle alongside sustained systemic administration of OR486 (15mg/kg/day) or vehicle over a 2-week period. Intrathecal delivered antagonist doses were selected based on their ability to block pain or related behaviors in other rat models when administered i.t.. 59-61 Similar to animals receiving vehicle, those receiving sustained i.t. administration of the non-selective βAR antagonist propranolol, the β 2 AR antagonist ICI-118,511, or the β 3 AR antagonist SR59230A alongside systemic OR486 exhibited mechanical allodynia (Fig 4A, F 2,159 =16.63, p<0.0001; Fig 4D, F 2,158 =16.60, p<0.0001; Fig 4G, F 2,173 =16.13, p<0.0001), mechanical hyperalgesia (Fig 4B, F 2,164 =9.149, p=0.0002; Fig 4E, F 2,165 =13.33, p<0.0001; Fig 4H, F 2,181 =6.544, p=0.0018) and thermal hyperalgesia (Fig 4C, F 2,164 =85.26, p<0.0001; Fig 4F, F 2,164 =86.01, p<0.0001; Fig 4I, F 2,178 =81.55, p<0.0001).…”

Section: Resultsmentioning

confidence: 99%

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

2016

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Background Patients with chronic pain disorders exhibit increased levels of catecholamines alongside diminished activity of catechol-O-methyltransferase (COMT), an enzyme that metabolizes catecholamines. The authors found that acute pharmacologic inhibition of COMT in rodents produces hypersensitivity to mechanical and thermal stimuli via β-adrenergic receptor (βAR) activation. The contribution of distinct βAR populations to the development of persistent pain linked to abnormalities in catecholamine signaling requires further investigation. Methods Here, the authors sought to determine the contribution of peripheral, spinal, and supraspinal βARs to persistent COMT-dependent pain. They implanted osmotic pumps to deliver the COMT inhibitor OR486 (Tocris, USA) for 2 weeks. Behavioral responses to mechanical and thermal stimuli were evaluated before and every other day after pump implantation. The site of action was evaluated in adrenalectomized rats receiving sustained OR486 or in intact rats receiving sustained βAR antagonists peripherally, spinally, or supraspinally alongside OR486. Results The authors found that male (N = 6) and female (N = 6) rats receiving sustained OR486 exhibited decreased paw withdrawal thresholds (control 5.74 ± 0.24 vs. OR486 1.54 ± 0.08, mean ± SEM) and increased paw withdrawal frequency to mechanical stimuli (control 4.80 ± 0.22 vs. OR486 8.10 ± 0.13) and decreased paw withdrawal latency to thermal heat (control 9.69 ± 0.23 vs. OR486 5.91 ± 0.11). In contrast, adrenalectomized rats (N = 12) failed to develop OR486-induced hypersensitivity. Furthermore, peripheral (N = 9), but not spinal (N = 4) or supraspinal (N = 4), administration of the nonselective βAR antagonist propranolol, the β2AR antagonist ICI-118,511, or the β3AR antagonist SR59230A blocked the development of OR486-induced hypersensitivity. Conclusions Peripheral adrenergic input is necessary for the development of persistent COMT-dependent pain, and peripherally-acting βAR antagonists may benefit chronic pain patients.

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“…The remaining IUGR lambs were randomly assigned to also receive either no postnatal intervention (IUGR; n = 14) or to receive daily oral ADRβ modifiers (IUGR-AR, n = 8). This daily treatment consisted of 20 µg kg −1 day −1 clenbuterol (ADRβ2 agonist), 400 µg kg −1 day −1 atenolol (ADRβ1 antagonist) and 2 µg kg −1 day −1 SR59230A J Physiol 597.24 (ADRβ3 antagonist), given orally in 50 ml of milk replacer (Coleman et al 1988;MacRae et al 1988;Manara et al 1996;Torneke et al 1998;Chiou et al 2000;Despres et al 2002;Kanzler et al 2011;Miniaci et al 2013). The doses of clenbuterol, atenolol and SR59230A were chosen to provide the lowest effective dose in order to minimize potential off-target effects.…”

Section: Ethical Approvalmentioning

confidence: 99%

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

Yates

Camacho

Kelly

et al. 2019

The Journal of Physiology

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Key points Previous studies in fetuses with intrauterine growth restriction (IUGR) have shown that adrenergic dysregulation was associated with low insulin concentrations and greater insulin sensitivity. Although whole‐body glucose clearance is normal, 1‐month‐old lambs with IUGR at birth have higher rates of hindlimb glucose uptake, which may compensate for myocyte deficiencies in glucose oxidation. Impaired glucose‐stimulated insulin secretion in IUGR lambs is due to lower intra‐islet insulin availability and not from glucose sensing. We investigated adrenergic receptor (ADR) β2 desensitization by administering oral ADRβ modifiers for the first month after birth to activate ADRβ2 and antagonize ADRβ1/3. In IUGR lambs ADRβ2 activation increased whole‐body glucose utilization rates and insulin sensitivity but had no effect on isolated islet or myocyte deficiencies. IUGR establishes risk for developing diabetes. In IUGR lambs we identified disparities in key aspects of glucose‐stimulated insulin secretion and insulin‐stimulated glucose oxidation, providing new insights into potential mechanisms for this risk. Abstract Placental insufficiency causes intrauterine growth restriction (IUGR) and disturbances in glucose homeostasis with associated β adrenergic receptor (ADRβ) desensitization. Our objectives were to measure insulin‐sensitive glucose metabolism in neonatal lambs with IUGR and to determine whether daily treatment with ADRβ2 agonist and ADRβ1/β3 antagonists for 1 month normalizes their glucose metabolism. Growth, glucose‐stimulated insulin secretion (GSIS) and glucose utilization rates (GURs) were measured in control lambs, IUGR lambs and IUGR lambs treated with adrenergic receptor modifiers: clenbuterol atenolol and SR59230A (IUGR‐AR). In IUGR lambs, islet insulin content and GSIS were less than in controls; however, insulin sensitivity and whole‐body GUR were not different from controls. Of importance, ADRβ2 stimulation with β1/β3 inhibition increases both insulin sensitivity and whole‐body glucose utilization in IUGR lambs. In IUGR and IUGR‐AR lambs, hindlimb GURs were greater but fractional glucose oxidation rates and ex vivo skeletal muscle glucose oxidation rates were lower than controls. Glucose transporter 4 (GLUT4) was lower in IUGR and IUGR‐AR skeletal muscle than in controls but GLUT1 was greater in IUGR‐AR. ADRβ2, insulin receptor, glycogen content and citrate synthase activity were similar among groups. In IUGR and IUGR‐AR lambs heart rates were greater, which was independent of cardiac ADRβ1 activation. We conclude that targeted ADRβ2 stimulation improved whole‐body insulin sensitivity but minimally affected defects in GSIS and skeletal muscle glucose oxidation. We show that risk factors for developing diabetes are independent of postnatal catch‐up growth in IUGR lambs as early as 1 month of age and are inherent to the islets and myocytes.

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Involvement of β3-adrenergic receptors in the control of food intake in rats

Cited by 17 publications

References 36 publications

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Possible Involvement of Beta-Adrenergic Receptors on Nociceptin/Orphanin FQ Induced Food Consumption in Male Rats

Persistent Catechol-O-methyltransferase–dependent Pain Is Initiated by Peripheral β-Adrenergic Receptors

Postnatal β2 adrenergic treatment improves insulin sensitivity in lambs with IUGR but not persistent defects in pancreatic islets or skeletal muscle

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