The orbitofrontal cortex, food intake and obesity

Abstract

Obesity is a major health challenge facing many people throughout the world. Increased consumption of palatable, high-caloric foods is one of the major drivers of obesity. Both orexigenic and anorexic states have been thoroughly reviewed elsewhere; here, we focus on the cognitive control of feeding in the context of obesity, and how the orbitofrontal cortex (OFC) is implicated, based on data from preclinical and clinical research. The OFC is important in decision-making and has been heavily researched in neuropsychiatric illnesses such as addiction and obsessive–compulsive disorder. However, activity in the OFC has only recently been described in research into food intake, obesity and eating disorders. The OFC integrates sensory modalities such as taste, smell and vision, and it has dense reciprocal projections into thalamic, midbrain and striatal regions to fine-tune decision-making. Thus, the OFC may be anatomically and functionally situated to play a critical role in the etiology and maintenance of excess feeding behaviour. We propose that the OFC serves as an integrative hub for orchestrating motivated feeding behaviour and suggest how its neurobiology and functional output might be altered in the obese state.

Fig. 1

Afferent and efferent projections from subregions of the rodent orbitofrontal cortex. BLA = basolateral amygdala; DLS = dorsolateral striatum; DMS = dorsomedial striatum; LH = lateral hypothalamus; lOFC = lateral orbitofrontal cortex; MC = motor cortex; mOFC = medial orbitofrontal cortex; NAc = nucleus accumbens; OC = olfactory cortex; SC = somatosensory cortex; STN = subthalamic nuclei; VC = visual cortex; vOFC = ventral orbitofrontal cortex; VTA = ventral tegmental area.