Amygdaloid-lesion hyperphagia: impaired response to caloric challenges and altered macronutrient selection

Abstract

Lesions of the most posterodorsal aspects of the amygdala in female rats result in hyperphagia and moderate obesity. In the present study, rats with amygdaloid lesions did not increase their daily food intake when their powdered diet was diluted with 25 or 50% nonnutritive bulk. Control animals adjusted their food intake appropriately. In a second study, rats with lesions ate less food (lab chow pellets) than controls when allowed to eat for only 1 h/day for 10 days. In experiment 3, rats were offered a three-choice macronutrient diet. Whereas four of six control animals preferred the high-fat diet, all eight of the rats with amygdaloid lesions displayed a distinct preference for the high-carbohydrate diet, including those that had preferred the high-fat diet before surgery. These results, along with the previous finding that identical lesions result in hyperinsulinemia, indicate that the amygdala is involved in both the homeostatic regulation of food (caloric) intake and the selection of macronutrients.

Glutamate Microinjected in the Posterodorsal Medial Amygdala Induces Subtle Increase in the Consumption of a Three‐Choice Macronutrient Self‐Selection Diet in Male Rats

“…It is also conceivable that lesions involving the ''posterodorsal amygdala'' and that induced hyperphagia (King et al, 1998(King et al, , 1999(King et al, , 2003Rollins and King, 2000;Grundmann et al, 2005) have affected other amygdaloid nuclei or transition areas besides the MePD (Rollins and King, 2000;King et al, 2003;Moscarello et al, 2009). In effect, excessive weight gains in lesioned females might be more related to damage the intra-amygdaloid division of the bed nucleus of the ST than to the MePD itself (King et al, 1998).…”

“…Previous reports involved the ''posterodorsal region'' of the amygdala with feeding behavior in rats (King et al, 1998(King et al, , 1999(King et al, , 2003Rollins and King, 2000;Grundmann et al, 2005). This wide area is neither an anatomical nor a functional unit; rather, it involves different amygdaloid components, such as the medial nucleus of the amygdala (MeA), the stria terminalis (ST), and the bed nucleus of the ST among others.…”

“…This wide area is neither an anatomical nor a functional unit; rather, it involves different amygdaloid components, such as the medial nucleus of the amygdala (MeA), the stria terminalis (ST), and the bed nucleus of the ST among others. Unilateral or bilateral electrolytic lesions of this ''posterodorsal region'' led Long-Evans adult female rats to display a marked preference for carbohydrate consumption, hyperphagia, and an abnormal increase in body weight (King et al, 1998(King et al, , 1999(King et al, , 2003. Lesions also promoted anterograde degeneration in the ipsilateral hypothalamic ventromedial nucleus (Rollins and King, 2000;Grundmann et al, 2005), an integrated area for the central control of food intake and energy balance (Berthoud, 2002).…”

Pituitary Adenylate Cyclase-Activating Peptide in the Central Amygdala Causes Anorexia and Body Weight Loss via the Melanocortin and the TrkB Systems

“…The central nucleus of the amygdala (CeA), considered part of the 'limbic' taste pathway, mediates the processing of emotional (rewarding and aversive) properties of stimuli including foods and may modulate hypothalamic activity by coupling sensory/affective processes to metabolic states (Kishi and Elmquist, 2005). The CeA, indeed, plays a key role in the non-homeostatic regulation of feeding and the regulation of macronutrient selection (King et al, 1998;Will et al, 2004). Rats with ablation of the CeA display a reduction in body weight as well as lower preferences for tasty solutions (Touzani et al, 1997), and the activation/inhibition of specific neuropeptide/hormone receptors or cell types within the CeA has been shown to modulate food intake, especially if palatable (Boghossian et al, 2009;Primeaux et al, 2006).…”

Genes involved in obesity: Adipocytes, brain and microflora

“…In fact, intra-PVN injection of NPY increases food intake, more specifically carbohydrate intake (Stanley et al, 1985). Arcuate NPY neurons also send innervation to amygdala, an area also involved in feeding behaviour since lesion of amygdala produces obesity and increases preference for high carbohydrate diet (King et al, 1998;King et al, 2003). When administrated into the amygdala, NPY selectively reduces high fat food intake and preference, without altering total caloric intake (Primeaux et al, 2006).…”