The Forebrain Is Not Essential for Sympathoadrenal Hyperglycemic Response to Glucoprivation

DiRocco, Richard J.; Grill, Harvey J.

doi:10.1126/science.451558

Cited by 151 publications

(64 citation statements)

References 52 publications

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“…In this case, a different population of catecholamine neurons was lesioned which disrupted the sympathoadrenal response to 2DG but left the feeding response intact. The latter result is consistent with a study cited above in which the sympathoadrenal response was observed in decerebrates (44). The abolition of the hyperphagic response to 2DG by DSAP into the PVN is consistent with the suggestion that this structure plays an obligate integrative role, and it is tempting to suggest further that the long-loop mechanism is also important for behavioral response to metabolic signals associated with natural deprivation.…”

Section: Toward An Interpretation Of the Deficient Response To Deprivsupporting

confidence: 92%

“…The decerebrate preparation can be used to address the potential for brainstem substrates to effect the same responses in isolation of forebrain influence. Decerebrate rats show a fully formed sympathoadrenal response to systemic 2DG administration (44), indicating that the brainstem contains a complete circuit, including interoceptors responsive to the reduction in utilizable glucose and sufficient integrative machinery to engage a descending command to spinal effectors. The ingestive behavioral response to metabolic inhibitors has not been evaluated.…”

Section: Interoceptor-driven Responsesmentioning

confidence: 99%

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The Neuroanatomical Axis for Control of Energy Balance

Grill

Kaplan

2002

Frontiers in Neuroendocrinology

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352

219

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The hypothalamic feeding-center model, articulated in the 1950s, held that the hypothalamus contains the interoceptors sensitive to blood-borne correlates of available or stored fuels as well as the integrative substrates that process metabolic and visceral afferent signals and issue commands to brainstem mechanisms for the production of ingestive behavior. A number of findings reviewed here, however, indicate that sensory and integrative functions are distributed across a central control axis that includes critical substrates in the basal forebrain as well as in the caudal brainstem. First, the interoceptors relevant to energy balance are distributed more widely than had been previously thought, with a prominent brainstem complement of leptin and insulin receptors, glucose-sensing mechanisms, and neuropeptide mediators. The physiological relevance of this multiple representation is suggested by the demonstration that similar behavioral effects can be obtained independently by stimulation of respective forebrain and brainstem subpopulations of the same receptor types (e.g., leptin, CRH, and melanocortin). The classical hypothalamic model is also challenged by the integrative achievements of the chronically maintained, supracollicular decerebrate rat. Decerebrate and neurologically intact rats show similar discriminative responses to taste stimuli and are similarly sensitive to intake-inhibitory feedback from the gut. Thus, the caudal brainstem, in neural isolation from forebrain influence, is sufficient to mediate ingestive responses to a range of visceral afferent signals. The decerebrate rat, however, does not show a hyperphagic response to food deprivation, suggesting that interactions between forebrain and brainstem are necessary for the behavioral response to systemic/ metabolic correlates of deprivation in the neurologically intact rat. At the same time, however, there is evidence suggesting that hypothalamic-neuroendocrine responses to fasting depend on pathways ascending from brainstem. Results reviewed are consistent with a distributionist (as opposed to hierarchical) model for the control of energy balance that emphasizes: (i) control mechanisms endemic to hypothalamus and brainstem that drive their unique effector systems on the basis of local interoceptive, and in the brainstem case, visceral, afferent inputs and (ii) a set of uni-and bidirectional interactions that coordinate adaptive neuroendocrine, autonomic, and behavioral responses to changes in metabolic status. KEY WORDS: feeding behavior; leptin; glucose sensing; decerebrate; neuropeptide; hypothalamic model; caudal brainstem; energy balance.

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Section: Toward An Interpretation Of the Deficient Response To Deprivsupporting

confidence: 92%

Section: Interoceptor-driven Responsesmentioning

confidence: 99%

The Neuroanatomical Axis for Control of Energy Balance

Grill

Kaplan

2002

Frontiers in Neuroendocrinology

Self Cite

352

219

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“…In addition, injections of 5-thio-glucose in different hypothalamic nuclei failed to induce a glucoregulatory response, whereas its injection into the NTS and the basolateral medulla region containing the A1/C1 catecholaminergic neurons, which project to different sites of the hypothalamus, induced a strong response. [54][55][56] Also, in decerebrated rats, the hyperglycemic response to an intraperitoneal injection of 2-DG is preserved, 57 and c-fos immunostaining revealed that the activated neurons are present in the NTS, the dorsal motor nucleus of the vagus and the catecholaminergic neurons of the basolateral medulla. 58 Thus, hypoglycemia can be detected at several sites, the hepatoportal vein area, the brainstem and the hypothalamus.…”

Section: S64mentioning

confidence: 94%

Glucose sensing and the pathogenesis of obesity and type 2 diabetes

Thorens

2008

Int J Obes

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The control of body weight and of blood glucose concentrations depends on the exquisite coordination of the function of several organs and tissues, in particular the liver, muscle and fat. These organs and tissues have major roles in the use and storage of nutrients in the form of glycogen or triglycerides and in the release of glucose or free fatty acids into the blood, in periods of metabolic needs. These mechanisms are tightly regulated by hormonal and nervous signals, which are generated by specialized cells that detect variations in blood glucose or lipid concentrations. The hormones insulin and glucagon not only regulate glycemic levels through their action on these organs and the sympathetic and parasympathetic branches of the autonomic nervous system, which are activated by glucose or lipid sensors, but also modulate pancreatic hormone secretion and liver, muscle and fat glucose and lipid metabolism. Other signaling molecules, such as the adipocyte hormones leptin and adiponectin, have circulating plasma concentrations that reflect the level of fat stored in adipocytes. These signals are integrated at the level of the hypothalamus by the melanocortin pathway, which produces orexigenic and anorexigenic neuropeptides to control feeding behavior, energy expenditure and glucose homeostasis. Work from several laboratories, including ours, has explored the physiological role of glucose as a signal that regulates these homeostatic processes and has tested the hypothesis that the mechanism of glucose sensing that controls insulin secretion by the pancreatic beta-cells is also used by other cell types. I discuss here evidence for these mechanisms, how they integrate signals from other nutrients such as lipids and how their deregulation may initiate metabolic diseases.

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“…CCK appears required for the ''satiety'' response [155], which also involves neurons in the NTS as well as the dorsomotor nucleus of the vagus (DMV), and is blocked by vagal deafferentiation [156]. In addition to meal size control, decerebrate rats also show a fully formed sympathoadrenal response to systemic 2DG administration [157], indicating that the brainstem houses a complete system responsive to glucoprivation. However, decerebrate rats are not able to increase meal size appropriately in response to food deprivation [158], and, therefore, have an inadequate response to a long-term homeostatic challenge, which requires interactions between hypothalamic and caudal brainstem nuclei [152].…”

Section: The Caudal Brainstem: Autonomic Control Of Eatingmentioning

confidence: 99%

Neuronal control of energy homeostasis

Gao¹,

Horváth²

2007

FEBS Letters

123

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Neuronal control of body energy homeostasis is the key mechanism by which animals and humans regulate their long-term energy balance. Various hypothalamic neuronal circuits (which include the hypothalamic melanocortin, midbrain dopamine reward and caudal brainstem autonomic feeding systems) control energy intake and expenditure to maintain body weight within a narrow range for long periods of a life span. Numerous peripheral metabolic hormones and nutrients target these structures providing feedback signals that modify the default ''settings'' of neuronal activity to accomplish this balance. A number of molecular genetic tools for manipulating individual components of brain energy homeostatic machineries, in combination with anatomical, electrophysiological, pharmacological and behavioral techniques, have been developed, which provide a means for elucidating the complex molecular and cellular mechanisms of feeding behavior and metabolism. This review will highlight some of these advancements and focus on the neuronal circuitries of energy homeostasis.

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The Forebrain Is Not Essential for Sympathoadrenal Hyperglycemic Response to Glucoprivation

Cited by 151 publications

References 52 publications

The Neuroanatomical Axis for Control of Energy Balance

The Neuroanatomical Axis for Control of Energy Balance

Glucose sensing and the pathogenesis of obesity and type 2 diabetes

Neuronal control of energy homeostasis

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