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* Although pharmacological studies have demonstrated β-endorphin (β-End) to stimulate feeding in variety of animals, recent demonstration of hyperphagia and obesity in β-End knockout male mice suggests that endogenous β-End may have anorexic effect in regulating energy homeostasis.
Abhiram Sahu. Endocrinology. First published March 24, 2004 as doi:10.1210/en.2004-0032
 | Adipocyte-derived-Factors
|  | | |  | | | |  | |  | |  | | Overproduction of adipocyte-derived factors and associated pathophysiological complications. LPL, lipoprotein lipase. | | | | 
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| Overproduction of adipocyte-derived factors and associated
pathophysiological complications. LPL, lipoprotein lipase | | | |  | | | |  | | | | 
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The body produces hormones that act through the brain to regulate short-
and
long-term appetite and also the body's metabolism. The diagram shows
the sources of several of the hormones now under intensive
investigation. |
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The diagram shows the sources of several of the hormones now
under intensive investigation.
Marx J. Science. 299, 846-849.
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| Many
different hormones control our weight and appetite. The discovery of
new peptide hormones, which suppresses appetite for up to 12 hours, may
lead to a better understanding of this complex control system | | | | | Hormones
that control eating such as, leptin and insulin (lower part of the
figure) circulate in the blood at concentrations proportional to
body-fat mass. They decrease appetite by inhibiting neurons (centre)
that produce the molecules NPY and AGRP, while stimulating
melanocortin-producing neurons in the arcuate-nucleus region of the
hypothalamus, near the third ventricle of the brain. NPY and AGRP
stimulate eating, and melanocortins inhibit eating, via other neurons
(top). Activation of NPY/AGRP-expressing neurons inhibits
melanocortin-producing neurons. The gastric hormone, ghrelin stimulates
appetite by activating the NPY/AGRP-expressing neurons. Batterham and
co-workers have shown that PYY (3-36), released from the colon, inhibits
these neurons and thereby decreases appetite for up to 12 hours. PYY
(3-36) works in part through the auto-inhibitory NPY receptor Y2R. Schwartz M.W. & Mortin G.J. Nature. 418 , 595 - 597 (2002). | | | | | |
| Central command Centers | | | | | The
arcuate nucleus (ARC) of the brain contains two sets of neurons with
opposing effects. Activation of the AGRP/NPY neurons increases appetite
and metabolism, whereas activation of the POMC/CART neurons has the
opposite effect. These neurons connect with second-order neurons in
other brain centers, and from there the signals are transmitted through
the nucleus tratus solitarius (NTS) to the body. Many
appetite-regulating hormones work through the ARC, although they may
have direct effects on the NTS and other brain centers as well. Schwartz M.W. & Mortin G.J. Nature. 418 , 595 - 597 (2002). | | | |  | | | | 
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References - Ghrelin induces adiposity in rodents.
Matthias Tscho?p, David L. Smiley & Mark L. Heiman, Nature, 407, 908-913 (October 19,2000).
- Identification of receptors for neuromedin U and its role in feeding.
Howard A. D., et al., Nature 406 , 70-75 (July 6, 2000)
- Alternative role for prolactin-releasing peptide in the regulation of food intake.
Lawrence CB, et al., Nat Neurosci 2000 Jul;3(7):645-646
- Obesity in the new millennium.
Friedman J. M., Nature 404, 632-634
- Centrol Nervous System Control of Food Intake.
Schwartz M. W. et al. , Nature 404, 661-671
- Medical Strategies in the treatment of obesity.
Bray G. A. and Tartagliat L. A., Nature 404,672-677
- Genetics of body-weight regulation.
Barsh G. S. et al., Nature 404,644-651
- Obesity as a medical Problem.
Kopelman P. G. Nature 404, 635-643
- Overweight, Obesity, and Mortality from Cancer in a Prospectively Studied Cohort of U.S. Adults
Calle EE, Rodriguez C, Walker-Thurmond, K, and Thun M J. New England J. of Med 2003 Apr: 348 (17): 1625-1638
- The emerging science of body weight regulation and its impact on obesity treatment.
Korner, J. and Aronne LJ. J. Clin. Invest. (2003). 111: 565-570
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