Oral Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2012

Fat and the brain - interactions between obesity, appetite and mood (#44)

Gilberto Paz-Filho 1
  1. Department of Translational Medicine at The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia

Overweight and obesity have reached epidemic proportions in Australia. Less than one third of the Australian adult population has normal weight 1.Obesity is a known risk factor for decreased brain tissue volume, cognitive impairment and Alzheimer’s disease 2. It is also associated with depression 3,decreased quality of life 4,and decreased executive function 5. These alterations could be attributed to the excess fat, or to the metabolic and cardiovascular changes that are seen in obese individuals, such as hypercortisolaemia, poor physical fitness, impaired respiratory function, pro-inflammatory state, dyslipidaemia, hyperglycaemia, insulin resistance and hypertension. Leptin is an adipokine produced mainly by the white adipose tissue, and it is increased in obesity. Leptin plays key roles not only in regulating food intake, but also in mood and cognition 6 by affecting neurogenesis, neural growth, and neural survival in brain areas other than the hypothalamus 7, 8 .

The regulation of human body weight, appetite and mood relies on sophisticate interactions between the central nervous system and the periphery. Food intake and energy expenditure are regulated by central and peripheral signals from the adipose tissue, gastrointestinal tract, and pancreas 9. Changes in adiposity, in turn, might also be associated with changes in mood and cognition, at least partially mediated by leptin.

The effects of excess fat mass and of the components of metabolic syndrome on mood, quality of life and executive function need to be better characterised, and correlated with the hormonal alterations that are seen in obesity and with the genetic polymorphisms known to predispose to mood and cognitive disorders. Ongoing studies will allow the development of prophylactic and therapeutic targets against obesity-associated mood and cognitive disorders.  

  1. ABS. National Health Survey: Summary of Results, 2007-2008.
  2. Siervo M, Arnold R, Wells JC, Tagliabue A, Colantuoni A, Albanese E, et al. Intentional weight loss in overweight and obese individuals and cognitive function: a systematic review and meta-analysis. Obes Rev. 2011 Nov;12(11):968-83.
  3. Bornstein SR, Schuppenies A, Wong ML, Licinio J. Approaching the shared biology of obesity and depression: the stress axis as the locus of gene-environment interactions. Mol Psychiatry. 2006 Oct;11(10):892-902.
  4. Dixon JB. The effect of obesity on health outcomes. Mol Cell Endocrinol. 2010 Mar 25;316(2):104-8.
  5. Gunstad J, Paul RH, Cohen RA, Tate DF, Spitznagel MB, Gordon E. Elevated body mass index is associated with executive dysfunction in otherwise healthy adults. Compr Psychiatry. 2007 Jan-Feb;48(1):57-61.
  6. Paz-Filho GJ, Babikian T, Asarnow R, Delibasi T, Esposito K, Erol HK, et al. Leptin replacement improves cognitive development. PLoS One. 2008;3(8):e3098.
  7. London ED, Berman SM, Chakrapani S, Delibasi T, Monterosso J, Erol HK, et al. Short-term plasticity of gray matter associated with leptin deficiency and replacement. J Clin Endocrinol Metab. 2011 Aug;96(8):E1212-20.
  8. Paz-Filho G, Wong ML, Licinio J. The procognitive effects of leptin in the brain and their clinical implications. Int J Clin Pract. 2010 Dec;64(13):1808-12.
  9. Boguszewski CL, Paz-Filho G, Velloso LA. Neuroendocrine body weight regulation: integration between fat tissue, gastrointestinal tract, and the brain. Endokrynol Pol. 2010 Mar-Apr;61(2):194-206.