Role of inferior olive and thoracic IML neurons in nonshivering thermogenesis in rats

Uno, Tadashi; Shibata, Masaaki

doi:10.1152/ajpregu.2001.280.2.r536

Cited by 29 publications

(28 citation statements)

References 29 publications

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“…In particular, GLP-1 binding sites were found in the inferior olive and nucleus of the solitary tract (9); both areas have been described as involved in the control of thermogenesis (40,41). Although at the central level SIRT1/p53 and AMPK pathways are interacting to mediate the orexigenic actions of ghrelin (33), neither SIRT1 nor p53 modified liraglutide-induced hypophagia or weight loss, indicating that the brain SIRT1/p53 system does not interact with AMPK to mediate the actions of liraglutide on thermogenesis and browning.…”

Section: Discussionmentioning

confidence: 99%

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

et al. 2014

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GLP-1 receptor (GLP-1R) is widely located throughout the brain, but the precise molecular mechanisms mediating the actions of GLP-1 and its long-acting analogs on adipose tissue as well as the brain areas responsible for these interactions remain largely unknown. We found that central injection of a clinically used GLP-1R agonist, liraglutide, in mice stimulates brown adipose tissue (BAT) thermogenesis and adipocyte browning independent of nutrient intake. The mechanism controlling these actions is located in the hypothalamic ventromedial nucleus (VMH), and the activation of AMPK in this area is sufficient to blunt both central liraglutide-induced thermogenesis and adipocyte browning. The decreased body weight caused by the central injection of liraglutide in other hypothalamic sites was sufficiently explained by the suppression of food intake. In a longitudinal study involving obese type 2 diabetic patients treated for 1 year with GLP-1R agonists, both exenatide and liraglutide increased energy expenditure. Although the results do not exclude the possibility that extrahypothalamic areas are also modulating the effects of GLP-1R agonists, the data indicate that long-acting GLP-1R agonists influence body weight by regulating either food intake or energy expenditure through various hypothalamic sites and that these mechanisms might be clinically relevant.

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Section: Discussionmentioning

confidence: 99%

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

et al. 2014

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“…In the midbrain, we found a high number of infected cells in the rubral, tegmental, and olivary areas. These areas also send descending projections to IBAT and have been linked to IBAT thermogenesis (52,56,58). For example, laboratory rats receiving procaine injections into the pedunculopontine tegmental nucleus or into the retrorubral field and rubrospinal tract increase T IBAT (51).…”

Section: Discussionmentioning

confidence: 99%

Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses

Vaughan

Bartness

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Vaughan CH, Bartness TJ. Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses. Am J Physiol Regul Integr Comp Physiol 302: R1049 -R1058, 2012. First published February 29, 2012 doi:10.1152/ajpregu.00640.2011.-Brown adipose tissue (BAT) thermogenic activity and growth are controlled by its sympathetic nervous system (SNS) innervation, but nerve fibers containing sensory-associated neuropeptides [substance P, calcitonin gene-related peptide (CGRP)] also suggest sensory innervation. The central nervous system (CNS) projections of BAT afferents are unknown. Therefore, we used the H129 strain of the herpes simplex virus-1 (HSV-1), an anterograde transneuronal viral tract tracer used to delineate sensory nerve circuits, to define these projections. HSV-1 was injected into interscapular BAT (IBAT) of Siberian hamsters and HSV-1 immunoreactivity (ir) was assessed 24, 48, 72, 96, and 114 h postinjection. The 96-and 114-h groups had the most HSV-1-ir neurons with marked infections in the hypothalamic paraventricular nucleus, periaqueductal gray, olivary areas, parabrachial nuclei, raphe nuclei, and reticular areas. These sites also are involved in sympathetic outflow to BAT suggesting possible BAT sensory-SNS thermogenesis feedback circuits. We tested the functional contribution of IBAT sensory innervation on thermogenic responses to an acute (24 h) cold exposure test by injecting the specific sensory nerve toxin capsaicin directly into IBAT pads and then measuring core (Tc) and IBAT (TIBAT) temperature responses. CGRP content was significantly decreased in capsaicin-treated IBAT demonstrating successful sensory nerve destruction. TIBAT and Tc were significantly decreased in capsaicin-treated hamsters compared with the saline controls at 2 h of cold exposure. Thus the central sensory circuits from IBAT have been delineated for the first time, and impairment of sensory feedback from BAT appears necessary for the appropriate, initial thermogenic response to acute cold exposure.herpes simplex virus-1; capsaicin; sensory afferents; iButton; body temperature; interscapular brown adipose tissue temperature; calcitonin gene-related peptide RECENT REPORTS of functional brown adipose tissue (BAT) in humans has sparked more interest in mapping the connections between BAT and the brain in the hope of increasing thermogenesis thereby enhancing energy expenditure and reversing or preventing obesity (18,59,61). BAT is the major effector tissue in rodent thermogenesis (for review see Ref. 10) controlled nearly exclusively by the sympathetic nervous system (SNS) drive to the tissue (for review see Ref. 5). Because of reports of sensory nerve-associated neuropeptides at the level of the BAT pad (23,24,43), the potential for reciprocal connections between BAT and the brain would thus create the possibility of SNS-sensory feedback loops to control the thermogenic activity of the tissue in response to varying environmental and physiological cha...

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“…In this context, a VMH-specific knockdown of SF1 reduced EE and BAT UCP1 expression in mice [47]. The VMH is also connected to other brainstem regions linked to the regulation of BAT NST, such as the raphe pallidus (RPa) and inferior olive (IO) [28,29,48,49]. Activation of BAT NST can be modulated in the VMH by glutamate, hydroxybutyrate, NA, serotonin and tryptophan [50][51][52], and by peripheral hormones.…”

Section: Autonomic Modulation Of Bat Thermogenesismentioning

confidence: 99%

Hypothalamic-autonomic control of energy homeostasis

et al. 2015

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Regulation of energy homeostasis is tightly controlled by the central nervous system (CNS). Several key areas such as the hypothalamus and brainstem receive and integrate signals conveying energy status from the periphery, such as leptin, thyroid hormones, and insulin, ultimately leading to modulation of food intake, energy expenditure (EE), and peripheral metabolism. The autonomic nervous system (ANS) plays a key role in the response to such signals, innervating peripheral metabolic tissues, including brown and white adipose tissue (BAT and WAT), liver, pancreas, and skeletal muscle. The ANS consists of two parts, the sympathetic and parasympathetic nervous systems (SNS and PSNS). The SNS regulates BAT thermogenesis and EE, controlled by central areas such as the preoptic area (POA) and the ventromedial, dorsomedial, and arcuate hypothalamic nuclei (VMH, DMH, and ARC). The SNS also regulates lipid metabolism in WAT, controlled by the lateral hypothalamic area (LHA), VMH, and ARC. Control of hepatic glucose production and pancreatic insulin secretion also involves the LHA, VMH, and ARC as well as the dorsal vagal complex (DVC), via splanchnic sympathetic and the vagal parasympathetic nerves. Muscle glucose uptake is also controlled by the SNS via hypothalamic nuclei such as the VMH. There is recent evidence of novel pathways connecting the CNS and ANS. These include the hypothalamic AMP-activated protein kinase-SNS-BAT axis which has been demonstrated to be a key modulator of thermogenesis. In this review, we summarize current knowledge of the role of the ANS in the modulation of energy balance.

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Role of inferior olive and thoracic IML neurons in nonshivering thermogenesis in rats

Cited by 29 publications

References 29 publications

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

GLP-1 Agonism Stimulates Brown Adipose Tissue Thermogenesis and Browning Through Hypothalamic AMPK

Anterograde transneuronal viral tract tracing reveals central sensory circuits from brown fat and sensory denervation alters its thermogenic responses

Hypothalamic-autonomic control of energy homeostasis

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