The role of melanocortin neuronal pathways in circadian biology: A new homeostatic output involving melanocortin-3 receptors?

K. Begriche, G. M. Sutton, J. Fang, A. A. Butler

Research output: Contribution to journalReview article

16 Citations (Scopus)

Abstract

Obesity, insulin resistance and increased propensity for type 2 diabetes and cardiovascular disease result from an imbalance between energy intake and expenditure. The cloning of genes involved in energy homeostasis produced a simple feedback model for the homeostatic regulation of adipose mass. Serum leptin secreted from adipocytes signals nutrient sufficiency, curbing appetite and supporting energy expenditure. A rapid decline in leptin during nutrient scarcity instigates adaptive mechanisms, including increased appetite and reduced energy expenditure. Hypothalamic melanocortin neurons are important mediators of this response, integrating inputs of energy status from leptin with other peripheral signals. While this feedback response prolongs survival during fasting, other mechanisms allowing the prediction of nutrient availability also confer a selective advantage. This adaptation has been commonly studied in rodents using restricted feeding paradigms constraining food intake to limited periods at 24-h intervals. Restricted feeding rapidly elicits rhythmic bouts of activity and wakefulness anticipating food presentation. While the response exhibits features suggesting a clock-like mechanism, the neuromolecular mechanisms governing expression of food anticipatory behaviours are poorly understood. Here we discuss a model whereby melanocortin neurons regulating the homeostatic adaptation to variable caloric availability also regulate inputs into neural networks governing anticipatory rhythms in wakefulness, activity and metabolism.

Original languageEnglish (US)
Pages (from-to)14-24
Number of pages11
JournalObesity Reviews
Volume10
Issue numberSUPPL. 2
DOIs
StatePublished - Nov 1 2009

Fingerprint

Receptor, Melanocortin, Type 3
Melanocortins
Food
Leptin
Energy Metabolism
Wakefulness
Appetite
Neurons
Energy Intake
Adipocytes
Type 2 Diabetes Mellitus
Insulin Resistance
Organism Cloning
Rodentia
Fasting
Homeostasis
Cardiovascular Diseases
Obesity
Eating
Serum

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Public Health, Environmental and Occupational Health

Cite this

@article{1d774de5ef434548b3aab8d67bda5a72,
title = "The role of melanocortin neuronal pathways in circadian biology: A new homeostatic output involving melanocortin-3 receptors?",
abstract = "Obesity, insulin resistance and increased propensity for type 2 diabetes and cardiovascular disease result from an imbalance between energy intake and expenditure. The cloning of genes involved in energy homeostasis produced a simple feedback model for the homeostatic regulation of adipose mass. Serum leptin secreted from adipocytes signals nutrient sufficiency, curbing appetite and supporting energy expenditure. A rapid decline in leptin during nutrient scarcity instigates adaptive mechanisms, including increased appetite and reduced energy expenditure. Hypothalamic melanocortin neurons are important mediators of this response, integrating inputs of energy status from leptin with other peripheral signals. While this feedback response prolongs survival during fasting, other mechanisms allowing the prediction of nutrient availability also confer a selective advantage. This adaptation has been commonly studied in rodents using restricted feeding paradigms constraining food intake to limited periods at 24-h intervals. Restricted feeding rapidly elicits rhythmic bouts of activity and wakefulness anticipating food presentation. While the response exhibits features suggesting a clock-like mechanism, the neuromolecular mechanisms governing expression of food anticipatory behaviours are poorly understood. Here we discuss a model whereby melanocortin neurons regulating the homeostatic adaptation to variable caloric availability also regulate inputs into neural networks governing anticipatory rhythms in wakefulness, activity and metabolism.",
author = "K. Begriche and Sutton, {G. M.} and J. Fang and Butler, {A. A.}",
year = "2009",
month = "11",
day = "1",
doi = "10.1111/j.1467-789X.2009.00662.x",
language = "English (US)",
volume = "10",
pages = "14--24",
journal = "Obesity Reviews",
issn = "1467-7881",
publisher = "Wiley-Blackwell",
number = "SUPPL. 2",

}

The role of melanocortin neuronal pathways in circadian biology : A new homeostatic output involving melanocortin-3 receptors? / Begriche, K.; Sutton, G. M.; Fang, J.; Butler, A. A.

In: Obesity Reviews, Vol. 10, No. SUPPL. 2, 01.11.2009, p. 14-24.

Research output: Contribution to journalReview article

TY - JOUR

T1 - The role of melanocortin neuronal pathways in circadian biology

T2 - A new homeostatic output involving melanocortin-3 receptors?

AU - Begriche, K.

AU - Sutton, G. M.

AU - Fang, J.

AU - Butler, A. A.

PY - 2009/11/1

Y1 - 2009/11/1

N2 - Obesity, insulin resistance and increased propensity for type 2 diabetes and cardiovascular disease result from an imbalance between energy intake and expenditure. The cloning of genes involved in energy homeostasis produced a simple feedback model for the homeostatic regulation of adipose mass. Serum leptin secreted from adipocytes signals nutrient sufficiency, curbing appetite and supporting energy expenditure. A rapid decline in leptin during nutrient scarcity instigates adaptive mechanisms, including increased appetite and reduced energy expenditure. Hypothalamic melanocortin neurons are important mediators of this response, integrating inputs of energy status from leptin with other peripheral signals. While this feedback response prolongs survival during fasting, other mechanisms allowing the prediction of nutrient availability also confer a selective advantage. This adaptation has been commonly studied in rodents using restricted feeding paradigms constraining food intake to limited periods at 24-h intervals. Restricted feeding rapidly elicits rhythmic bouts of activity and wakefulness anticipating food presentation. While the response exhibits features suggesting a clock-like mechanism, the neuromolecular mechanisms governing expression of food anticipatory behaviours are poorly understood. Here we discuss a model whereby melanocortin neurons regulating the homeostatic adaptation to variable caloric availability also regulate inputs into neural networks governing anticipatory rhythms in wakefulness, activity and metabolism.

AB - Obesity, insulin resistance and increased propensity for type 2 diabetes and cardiovascular disease result from an imbalance between energy intake and expenditure. The cloning of genes involved in energy homeostasis produced a simple feedback model for the homeostatic regulation of adipose mass. Serum leptin secreted from adipocytes signals nutrient sufficiency, curbing appetite and supporting energy expenditure. A rapid decline in leptin during nutrient scarcity instigates adaptive mechanisms, including increased appetite and reduced energy expenditure. Hypothalamic melanocortin neurons are important mediators of this response, integrating inputs of energy status from leptin with other peripheral signals. While this feedback response prolongs survival during fasting, other mechanisms allowing the prediction of nutrient availability also confer a selective advantage. This adaptation has been commonly studied in rodents using restricted feeding paradigms constraining food intake to limited periods at 24-h intervals. Restricted feeding rapidly elicits rhythmic bouts of activity and wakefulness anticipating food presentation. While the response exhibits features suggesting a clock-like mechanism, the neuromolecular mechanisms governing expression of food anticipatory behaviours are poorly understood. Here we discuss a model whereby melanocortin neurons regulating the homeostatic adaptation to variable caloric availability also regulate inputs into neural networks governing anticipatory rhythms in wakefulness, activity and metabolism.

UR - http://www.scopus.com/inward/record.url?scp=70449411697&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70449411697&partnerID=8YFLogxK

U2 - 10.1111/j.1467-789X.2009.00662.x

DO - 10.1111/j.1467-789X.2009.00662.x

M3 - Review article

C2 - 19849798

AN - SCOPUS:70449411697

VL - 10

SP - 14

EP - 24

JO - Obesity Reviews

JF - Obesity Reviews

SN - 1467-7881

IS - SUPPL. 2

ER -