Hypothalamic neuropeptide mechanisms for regulating energy balance: from rodent models to human obesity

J. G. Mercer, John Roger Speakman

Research output: Contribution to journalArticle

84 Citations (Scopus)

Abstract

In small rodents there is compelling evidence of a lipostatic system of body mass regulation in which peripheral signals of energy storage are decoded in the hypothalamus. The ability of small mammals to defend an appropriate mass against imposed energy imbalance has implicated hypothalamic neuroendocrine systems in body mass regulation. The effect of the neuropeptide systems involved in this regulation is primarily compensatory. However, small mammals can also effect changes in the level of body mass that they will defend, as exemplified by seasonal species. Regulatory control over fat mass may be relatively loose in humans; the sizes of long-term storage depots may not themselves be regulated, but rather may be a consequence of temporal variations in the matching of supply and demand. Whether food intake is regulated to match energy demand, or to match demand and to regulate storage, it is clear that physiological defects or genetic variation in hypothalamic and peripheral feedback systems will have profound implications for fat storage. Study of mechanisms implicated in energy homeostasis in laboratory rodents is likely to continue to identify targets for pharmacological manipulation in the management of human obesity. (C) 2001 Elsevier Science Ltd. All rights reserved.

Original languageEnglish
Pages (from-to)101-116
Number of pages15
JournalNeuroscience & Biobehavioral Reviews
Volume25
DOIs
Publication statusPublished - 2001

Keywords

  • body mass
  • body weight
  • body weight set point
  • Siberian hamster
  • phodopus
  • photoperiod
  • hypothalamic neuropeptides
  • leptin
  • melanocortin
  • RECEPTOR MESSENGER-RNA
  • BODY-WEIGHT REGULATION
  • MELANIN-CONCENTRATING HORMONE
  • AGOUTI-RELATED PROTEIN
  • FORM SPLICE VARIANT
  • EARLY-ONSET OBESITY
  • DIET-INDUCED OBESE
  • LOW-FAT CONSUMERS
  • LEPTIN RECEPTOR
  • PREDATION RISK

Cite this

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title = "Hypothalamic neuropeptide mechanisms for regulating energy balance: from rodent models to human obesity",
abstract = "In small rodents there is compelling evidence of a lipostatic system of body mass regulation in which peripheral signals of energy storage are decoded in the hypothalamus. The ability of small mammals to defend an appropriate mass against imposed energy imbalance has implicated hypothalamic neuroendocrine systems in body mass regulation. The effect of the neuropeptide systems involved in this regulation is primarily compensatory. However, small mammals can also effect changes in the level of body mass that they will defend, as exemplified by seasonal species. Regulatory control over fat mass may be relatively loose in humans; the sizes of long-term storage depots may not themselves be regulated, but rather may be a consequence of temporal variations in the matching of supply and demand. Whether food intake is regulated to match energy demand, or to match demand and to regulate storage, it is clear that physiological defects or genetic variation in hypothalamic and peripheral feedback systems will have profound implications for fat storage. Study of mechanisms implicated in energy homeostasis in laboratory rodents is likely to continue to identify targets for pharmacological manipulation in the management of human obesity. (C) 2001 Elsevier Science Ltd. All rights reserved.",
keywords = "body mass, body weight, body weight set point, Siberian hamster, phodopus, photoperiod, hypothalamic neuropeptides, leptin, melanocortin, RECEPTOR MESSENGER-RNA, BODY-WEIGHT REGULATION, MELANIN-CONCENTRATING HORMONE, AGOUTI-RELATED PROTEIN, FORM SPLICE VARIANT, EARLY-ONSET OBESITY, DIET-INDUCED OBESE, LOW-FAT CONSUMERS, LEPTIN RECEPTOR, PREDATION RISK",
author = "Mercer, {J. G.} and Speakman, {John Roger}",
year = "2001",
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AU - Speakman, John Roger

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N2 - In small rodents there is compelling evidence of a lipostatic system of body mass regulation in which peripheral signals of energy storage are decoded in the hypothalamus. The ability of small mammals to defend an appropriate mass against imposed energy imbalance has implicated hypothalamic neuroendocrine systems in body mass regulation. The effect of the neuropeptide systems involved in this regulation is primarily compensatory. However, small mammals can also effect changes in the level of body mass that they will defend, as exemplified by seasonal species. Regulatory control over fat mass may be relatively loose in humans; the sizes of long-term storage depots may not themselves be regulated, but rather may be a consequence of temporal variations in the matching of supply and demand. Whether food intake is regulated to match energy demand, or to match demand and to regulate storage, it is clear that physiological defects or genetic variation in hypothalamic and peripheral feedback systems will have profound implications for fat storage. Study of mechanisms implicated in energy homeostasis in laboratory rodents is likely to continue to identify targets for pharmacological manipulation in the management of human obesity. (C) 2001 Elsevier Science Ltd. All rights reserved.

AB - In small rodents there is compelling evidence of a lipostatic system of body mass regulation in which peripheral signals of energy storage are decoded in the hypothalamus. The ability of small mammals to defend an appropriate mass against imposed energy imbalance has implicated hypothalamic neuroendocrine systems in body mass regulation. The effect of the neuropeptide systems involved in this regulation is primarily compensatory. However, small mammals can also effect changes in the level of body mass that they will defend, as exemplified by seasonal species. Regulatory control over fat mass may be relatively loose in humans; the sizes of long-term storage depots may not themselves be regulated, but rather may be a consequence of temporal variations in the matching of supply and demand. Whether food intake is regulated to match energy demand, or to match demand and to regulate storage, it is clear that physiological defects or genetic variation in hypothalamic and peripheral feedback systems will have profound implications for fat storage. Study of mechanisms implicated in energy homeostasis in laboratory rodents is likely to continue to identify targets for pharmacological manipulation in the management of human obesity. (C) 2001 Elsevier Science Ltd. All rights reserved.

KW - body mass

KW - body weight

KW - body weight set point

KW - Siberian hamster

KW - phodopus

KW - photoperiod

KW - hypothalamic neuropeptides

KW - leptin

KW - melanocortin

KW - RECEPTOR MESSENGER-RNA

KW - BODY-WEIGHT REGULATION

KW - MELANIN-CONCENTRATING HORMONE

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KW - DIET-INDUCED OBESE

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KW - LEPTIN RECEPTOR

KW - PREDATION RISK

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DO - 10.1016/S0149-7634(00)00053-1

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JO - Neuroscience & Biobehavioral Reviews

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