Cognitive and neuronal systems underlying obesity

• Published in: Physiology & behavior Vol. 106; no. 3; pp. 337 - 344
• Main Author: Kanoski, Scott E
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Amsterdam Elsevier Inc 06.06.2012; Elsevier
• Subjects: Animals; Behavioral psychophysiology; Biological and medical sciences; Brain; Brain - pathology; Carbohydrates; cognition; Cognition Disorders - etiology; Cognitive ability; Diets; Eating - physiology; Energy balance; Energy intake; Feeding behavior; Food; Food consumption; Food intake; foods; Fundamental and applied biological sciences. Psychology; Ghrelin; Hippocampus; Humans; Hyperphagia; Learning; Leptin; Medical sciences; Memory; Metabolic diseases; Neurons - pathology; Obesity; Obesity - complications; Obesity - epidemiology; Obesity - pathology; overeating; Psychiatry; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rat; Saturated fat; saturated fats; VTA; Western diet; Western diets; United States; Learning; VTA; Rat; Ghrelin; Leptin; Saturated fat; Hippocampus; Western diet; Central nervous system; Lipids; Encephalon; Acquisition process; Nutritional status; Obesity; Rodentia; Nutrition disorder; Adipokine; Cognitive system; Feeding; Appetite stimulant; Vertebrata; Mammalia; Diet; Saturated fatty acid; Animal
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/j.physbeh.2012.01.007

Abstract Since the late 1970s obesity prevalence and per capita food intake in the USA have increased dramatically. Understanding the mechanisms underlying the hyperphagia that drives obesity requires focus on the cognitive processes and neuronal systems controlling feeding that occurs in the absence of metabolic need (i.e., “non-homeostatic” intake). Given that a portion of the increased caloric intake per capita since the late 1970s is attributed to increased meal and snack frequency, and given the increased pervasiveness of environmental cues associated with energy dense, yet nutritionally depleted foods, there's a need to examine the mechanisms through which food-related cues stimulate excessive energy intake. Here, learning and memory principles and their underlying neuronal substrates are discussed with regard to stimulus-driven food intake and excessive energy consumption. Particular focus is given to the hippocampus, a brain structure that utilizes interoceptive cues relevant to energy status (e.g., neurohormonal signals such as leptin) to modulate stimulus-driven food procurement and consumption. This type of hippocampal-dependent modulatory control of feeding behavior is compromised by consumption of foods common to Western diets, including saturated fats and simple carbohydrates. The development of more effective treatments for obesity will benefit from a more complete understanding of the complex interaction between dietary, environmental, cognitive, and neurophysiological mechanisms contributing to excessive food intake.