Obesity/Bibliography

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Reviews

• Shively CA, Register TC, Clarkson TB (2009). "Social stress, visceral obesity, and coronary artery atherosclerosis: product of a primate adaptation". Am J Primatol 71 (9): 742-51. DOI:10.1002/ajp.20706. PMID 19452515. Research Blogging. ^[e]

• Crowley VEE et al. (2002) Obesity therapy: Altering the energy intake-and- expenditure balance sheet. Nature Reviews Drug Discovery 1:276-286
• Hill, JO. Peters, JC. (1998) Environmental contributions to the obesity epidemic. Science 280, 1371–4
• Grill, HJ. & Kaplan, JM. (2002) The neuroanatomical axis for control of energy balance. Front. Neuroendocrinol 23:2–40
• Berthoud, HR. (2002) Multiple neural systems controlling food intake and body weight. Neurosci. Biobehav. Rev 26:393–428
• Schwartz, MW. et al.(2000) Central nervous system control of food intake. Nature 404:661–71
• Speakman JR, Levitsky DA, Allison DB et al. (2011) Set points, settling points and some alternative models: theoretical options to understand how genes and environments combine to regulate body adiposity. Dis Model Mech 4:733-45.
  • Abstract: The close correspondence between energy intake and expenditure over prolonged time periods, coupled with an apparent protection of the level of body adiposity in the face of perturbations of energy balance, has led to the idea that body fatness is regulated via mechanisms that control intake and energy expenditure. Two models have dominated the discussion of how this regulation might take place. The set point model is rooted in physiology, genetics and molecular biology, and suggests that there is an active feedback mechanism linking adipose tissue (stored energy) to intake and expenditure via a set point, presumably encoded in the brain. This model is consistent with many of the biological aspects of energy balance, but struggles to explain the many significant environmental and social influences on obesity, food intake and physical activity. More importantly, the set point model does not effectively explain the 'obesity epidemic'--the large increase in body weight and adiposity of a large proportion of individuals in many countries since the 1980s. An alternative model, called the settling point model, is based on the idea that there is passive feedback between the size of the body stores and aspects of expenditure. This model accommodates many of the social and environmental characteristics of energy balance, but struggles to explain some of the biological and genetic aspects. The shortcomings of these two models reflect their failure to address the gene-by-environment interactions that dominate the regulation of body weight. We discuss two additional models--the general intake model and the dual intervention point model--that address this issue and might offer better ways to understand how body fatness is controlled.

Leptin

• Cowley, MA. et al.(2001) Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. Nature 411:480–484
• Farooqi IS et al. (1999). Effects of recombinant leptin therapy in a child with congenital leptin deficiency. New Eng J Med 341:879-84
• Montague CT, et al. Congenital leptin deficiency is associated with severe early- onset obesity in humans. Nature 387:903-8 (1997).
• Rafael J, Herling AW (2000) Leptin effect in ob/ob mice under thermoneutral conditions depends not necessarily on central satiation Am J Physiol 278:R790–5 PMID 10712302 url=http://ajpregu.physiology.org/cgi/content/full/278/3/R790#Top}}"Reduction of body mass in leptin-treated ob/ob mice was faster than in pair-fed ob/ob controls" (Free full text)

Ghrelin

• Kojima M et al. (1999) Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 402:656-60
• Cowley MA et al. (2003) The distribution and mechanism of action of ghrelin in the CNS demonstrates a novel hypothalamic circuit regulating energy homeostasis. Neuron 37:550-3
• Tschöp M, Smiley DL, & Heiman ML Ghrelin induces adiposity in rodents. Nature 407:908-13 (2000)

PPY

• Batterham RL et al. (2002)Gut hormone PYY3-36 physiologically inhibits food intake. Nature 418:650-4

IL6

• Wallenius V et al. (2002) Interleukin-6-deficient mice develop mature-onset obesity. Nature Medicine 8:75-79

Insulin

• Bruning JC et al. (2000) Role of brain insulin receptor in control of body weight and reproduction. Science 289:2122-5
• Obici, S et al.(2002) Decreasing hypothalamic insulin receptors causes hyperphagia and insulin resistance in rats. Nature Neurosci 5:566–72

MSH

• Fan W et al. (1997) Role of melanocortinergic neurons in feeding and the agouti obesity syndrome. Nature 385:165–8
• Lu D et al. (1994) Agouti protein is an antagonist of the melanocyte-stimulating-hormone receptor. Nature 371:799–802
• Huszar D et al. (1997) Targeted disruption of the melanocortin-4 receptor results in obesity in mice. Cell 88:131–41
• Seeley R et al. (1997) Melanocortin receptors in leptin effects. Nature 390:349