Toward a new neurobiology of energy balance, appetite, and obesity: The anatomists weigh in

Sawchenko, Paul E.

doi:10.1002/(sici)1096-9861(19981228)402:4<435::aid-cne1>3.0.co;2-m

Cited by 232 publications

(83 citation statements)

References 61 publications

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“…We paid particular attention to the POMC-derived aMSH projections to the paraventricular nucleus of the hypothalamus (PVH) because of their well-established importance in the neural control of food intake and energy balance (Ellacott and Cone, 2006; Elmquist et al, 2005; Gao and Horvath, 2007; Sawchenko, 1998). Although the overall distribution of aMSH-IR fibers was quite similar between mutant mice and control animals, clear differences were apparent in the density of the labeled fibers.…”

Section: Resultsmentioning

confidence: 99%

“…Appetite, energy balance, and metabolism are carefully regulated by the central nervous system (CNS) (see Elmquist et al, 2005; Gao and Horvath, 2007; Sawchenko, 1998 for reviews). The important components of this neural network include neurons located in the arcuate nucleus of the hypothalamus (ARH), particularly neurons producing proopiomelanocortin (POMC).…”

Section: Introductionmentioning

confidence: 99%

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Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation

et al. 2012

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Summary The hypothalamic melanocortin system, which includes neurons that produce proopiomelanocortin (POMC)-derived peptides, is a major negative regulator of energy balance. POMC neurons begin to acquire their unique properties during neonatal life. The formation of functional neural systems requires massive cytoplasmic remodeling that may involve autophagy, an important intracellular mechanism for the degradation of damaged proteins and organelles. Here we investigated the functional and structural effects of the deletion of an essential autophagy gene, Atg7, in POMC neurons. Lack of Atg7 in POMC neurons caused higher post-weaning body weight, increased adiposity, and glucose intolerance. These metabolic impairments were associated with an age-dependant accumulation of ubiquitin/p62-positive aggregates in the hypothalamus and a disruption in the maturation of POMC-containing axonal projections. Together, these data provide direct genetic evidence that Atg7 in POMC neurons is required for normal metabolic regulation and neural development, and they implicate hypothalamic autophagy deficiency in the pathogenesis of obesity.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation

et al. 2012

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“…Limbic efferents also innervate the mediobasal hypothalamus, including the arcuate nucleus 87 (Figure 3), which is a key regulator of energy balance and uses the PVN as a down-stream effector to regulate feeding and energy expenditure (via neuropeptidergic and GABAergic projections) 88 . The net output from the arcuate to the PVN is complex, communicating both orexigenic (neuropeptide Y, Agouti-related peptide) and anorexic (e.g., alpha-MSH) 88 signals.…”

Section: Middle Management Of Stress Responsesmentioning

confidence: 99%

“…The net output from the arcuate to the PVN is complex, communicating both orexigenic (neuropeptide Y, Agouti-related peptide) and anorexic (e.g., alpha-MSH) 88 signals. Notably, many of these peptides activate the HPA axis, implying that both positive and negative energy balance represent homeostatic stressors 89 .…”

Section: Middle Management Of Stress Responsesmentioning

confidence: 99%

Neural regulation of endocrine and autonomic stress responses

2009

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Preface The survival and well-being of all species requires appropriate physiological responses to environmental and homeostatic challenges. The reestablishment and maintenance of homeostasis entails the coordinate activation and control of neuroendocrine and autonomic stress systems. These collective stress responses are mediated via largely overlapping circuits in the limbic forebrain, hypothalamus and brainstem, so that the respective contribution of the neuroendocrine and autonomic systems is tuned in accordance with stressor modality or intensity. Limbic regions that are responsible for regulating stress responses intersect with circuits that are responsible for memory and reward, providing a means to tailor the stress response with respect to prior experience and anticipated outcomes.

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“…However, the roles and mechanisms of LHA neurons in regulation of feeding behavior have remained unclear. One of the widely accepted current understandings about the role of the LHA in the regulation of feeding is that it provides output from the hypothalamus to control appetite and metabolic rate, by sending information to various regions of the brain [7]. Included in these projections are orexin- and melanin concentrating hormone (MCH)-producing neurons, which are distinct populations of neurons distributed in and around the LHA, and both project diffusely to the entire central nervous system [8,9].…”

Section: Introductionmentioning

confidence: 99%

QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

et al. 2016

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How the hypothalamus transmits hunger information to other brain regions to govern whole brain function to orchestrate feeding behavior has remained largely unknown. Our present study suggests the importance of a recently found lateral hypothalamic neuropeptide, QRFP, in this signaling. Qrfp-/- mice were hypophagic and lean, and exhibited increased anxiety-like behavior, and were hypoactive in novel circumstances as compared with wild type littermates. They also showed decreased wakefulness time in the early hours of the dark period. Histological studies suggested that QRFP neurons receive rich innervations from neurons in the arcuate nucleus which is a primary region for sensing the body’s metabolic state by detecting levels of leptin, ghrelin and glucose. These observations suggest that QRFP is an important mediator that acts as a downstream mediator of the arcuate nucleus and regulates feeding behavior, mood, wakefulness and activity.

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Toward a new neurobiology of energy balance, appetite, and obesity: The anatomists weigh in

Cited by 232 publications

References 61 publications

Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation

Loss of Autophagy in Pro-opiomelanocortin Neurons Perturbs Axon Growth and Causes Metabolic Dysregulation

Neural regulation of endocrine and autonomic stress responses

QRFP-Deficient Mice Are Hypophagic, Lean, Hypoactive and Exhibit Increased Anxiety-Like Behavior

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