Energy homeostasis, obesity and eating disorders: recent advances in endocrinology.

Health problems resulting from obesity could offset many of the recent health gains achieved by modern medicine, and obesity may replace tobacco as the number one health risk for developed societies. An estimated 300,000 deaths per year and significant morbidity are directly attributable to obesity, mainly due to heart disease, diabetes, cancer, asthma, sleep apnea, arthritis, reproductive complications and psychological disturbances. In parallel with the increasing prevalence of obesity, there has been a dramatic increase in the number of scientific and clinical studies on the control of energy homeostasis and the pathogenesis of obesity to further our understanding of energy balance. It is now recognized that there are many central and peripheral factors involved in energy homeostasis, and it is expected that the understanding of these mechanisms should lead to effective treatments for the control of obesity. This brief review discusses the potential role of several recently discovered molecular pathways involved in the control of energy homeostasis, obesity and eating disorders.

[1]  V. Castracane,et al.  Leptin and Reproduction , 2012 .

[2]  Mohammad A Ghatei,et al.  Inhibition of food intake in obese subjects by peptide YY3-36. , 2003, The New England journal of medicine.

[3]  R. Leibel,et al.  To eat or not to eat - how the gut talks to the brain. , 2003, The New England journal of medicine.

[4]  E. Ravussin,et al.  The insulin-sensitizing role of the fat derived hormone adiponectin. , 2003, Current pharmaceutical design.

[5]  J. Chan,et al.  The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men. , 2003, The Journal of clinical investigation.

[6]  Pedro Iglesias,et al.  The role of the novel adipocyte-derived hormone adiponectin in human disease. , 2003, European journal of endocrinology.

[7]  Graham M Lord,et al.  Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. , 2002, The Journal of clinical investigation.

[8]  Rachel L. Batterham,et al.  Gut hormone PYY3-36 physiologically inhibits food intake , 2002, Nature.

[9]  S. Heymsfield,et al.  Low dose leptin administration reverses effects of sustained weight-reduction on energy expenditure and circulating concentrations of thyroid hormones. , 2002, The Journal of clinical endocrinology and metabolism.

[10]  J. Chan,et al.  Leptin and reproduction: a review. , 2002, Fertility and sterility.

[11]  R. Leibel,et al.  Leptin Regulation of Agrp and Npy mRNA in the Rat Hypothalamus , 2001, Journal of neuroendocrinology.

[12]  T. Funahashi,et al.  Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys. , 2001, Diabetes.

[13]  H. Sul,et al.  A Cysteine-rich Adipose Tissue-specific Secretory Factor Inhibits Adipocyte Differentiation* , 2001, The Journal of Biological Chemistry.

[14]  M. Lazar,et al.  The hormone resistin links obesity to diabetes , 2001, Nature.

[15]  M. Nakazato,et al.  A role for ghrelin in the central regulation of feeding , 2001, Nature.

[16]  S. Bloom,et al.  The novel hypothalamic peptide ghrelin stimulates food intake and growth hormone secretion. , 2000, Endocrinology.

[17]  F. Peale,et al.  FIZZ1, a novel cysteine‐rich secreted protein associated with pulmonary inflammation, defines a new gene family , 2000, The EMBO journal.

[18]  M. Nakazato,et al.  Ghrelin is a growth-hormone-releasing acylated peptide from stomach , 1999, Nature.

[19]  A. Prentice,et al.  Effects of recombinant leptin therapy in a child with congenital leptin deficiency. , 1999, The New England journal of medicine.

[20]  J. Halaas,et al.  Leptin and the regulation of body weight in mammals , 1998, Nature.

[21]  J. Flier,et al.  Obesity and the Hypothalamus: Novel Peptides for New Pathways , 1998, Cell.

[22]  N. Ling,et al.  Expression and characterization of a putative high affinity human soluble leptin receptor. , 1997, Endocrinology.

[23]  Rene Devos,et al.  Identification and expression cloning of a leptin receptor, OB-R , 1995, Cell.

[24]  S. Woods,et al.  A comparison between effects of intraventricular insulin and intraperitoneal lithium chloride on three measures sensitive to emetic agents. , 1995, Behavioral neuroscience.

[25]  M. Maffei,et al.  Positional cloning of the mouse obese gene and its human homologue , 1994, Nature.

[26]  N. Geary Pancreatic glucagon signals postprandial satiety , 1990, Neuroscience & Biobehavioral Reviews.

[27]  D. Dorsa,et al.  Insulin and insulin-like growth factors in the CNS , 1988, Trends in Neurosciences.

[28]  V. Mutt,et al.  Isolation of two novel candidate hormones using a chemical method for finding naturally occurring polypeptides , 1980, Nature.

[29]  E. Rolls,et al.  Bombesin suppresses feeding in rats , 1979, Nature.

[30]  D. Porte,et al.  The significance of basal insulin levels in the evaluation of the insulin response to glucose in diabetic and nondiabetic subjects. , 1967, The Journal of clinical investigation.

[31]  Printed in U.S.A. Copyright © 2003 by The Endocrine Society doi: 10.1210/en.2003-0241 Minireview: From Anorexia to Obesity—The Yin and Yang of Body Weight Control , 2022 .

[32]  H. Grill,et al.  Printed in U.S.A. Copyright © 2002 by The Endocrine Society Evidence That the Caudal Brainstem Is a Target for the Inhibitory Effect of Leptin on Food Intake , 2022 .