Obesity and the limbic system

doi:10.15406/jnsk.2023.13.00536

Journal of

eISSN: 2373-6410

Neurology & Stroke

Editorial Volume 13 Issue 1

Obesity and the limbic system

Stavros J Baloyannis

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Aristotelian University, Research Institute for Alzheimer’s disease, Greece

Correspondence: Stavros J Baloyannis, Professor Emeritus, Aristotelia Univesity, Angelaki 5, Thessaloniki 54621, Greece, Tel +302310270434, Fax +302310270434

Received: February 23, 2023 | Published: February 24, 2023

Citation: Baloyannis SJ. Obesity and the limbic system. J Neurol Stroke. 2023;13(1):12-14. DOI: 10.15406/jnsk.2023.13.00536

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Keywords

Obesity, limbic system, hypothalamus, amygdala neurotransmitters, BDNF

Editorial

Obesity is a serious multifactorial health problem, which has taken considerable dimensions in countries with a western style of diet.^1,2 It is reasonable, that the etiopathogenetic mechanisms of obesity are subjects for research in many fields of biological sciences in an attempt to improve the quality of life and prolong the viability, given that obesity may become a serious risk factor for several other co-morbidities affecting the life expectancy.^3–6

Although the genetic background and many environmental conditions may contribute to obesity,^7,8 the limbic system and hypothalamus must play a crucial role in the equilibrium of body weight and food intake,^9–11 since they control energy homeostasis,¹² in close collaboration with the peptides of the alimentary system, harmonizing the deposition of adipose tissue in the body,^13,14 according to food intake and energy consumption.

The hypothalamus, which is located on the floor of the third ventricle,¹⁵ among many other vital capacities,^16–18 is responsible for controlling energy balance and adjusting body weight.¹⁸ Theoretically, a ‘hunger center’ might exist in the lateral hypothalamus,¹⁹ been counteracted by a ‘satiety center’ in the ventromedial hypothalamic nucleus (VMN).^{20, 21} Nevertheless, many more areas of the brain, such as the amygdala, some hypothalamic nuclei, and mesencephalic neuronal networks are continuously involved in the desire for food intake and the regulation of body weight.²¹ However, it must be underlined that a high-lipid diet may increase the level of the inflammatory cytokines, inducing a chronic low-grade inflammatory reaction in the hypothalamus,^22,23characterized by astrocytic proliferation and activation of microglial cells and macrophages, a fact which was proved at the experimental level.^24,25

Loss of body weight control coincides, several times, with alterations of the amygdala^26–28 in connexion with the ventromedial hypothalamic nuclei, inducing hyperphagia,^29,30 hypometabolism, change of autonomic balance, and deficiency of growth hormone (GH), resulting eventually in the increase of body weight.³¹ The numerous connections of the hypothalamus with most of the cortical and subcortical structures of the brain and the cerebellum play a substantial role in the influence of mental and emotional activities upon the hypothalamic homeostatic regulation,³² with obvious consequences on the control of the body weight.³³Besides, many gut hormones and among them cholecystokinin, somatostatins, amylin, ghrelin, oxyntomodulin, glucagon-like peptide-2, and glucose-dependent insulinotropic peptide contribute greatly to the adjustment of body weight,³⁴ since they play a role of neurotransmitters, which control food intake and energy balance.³⁵

The dorsal vagal complex contributes greatly to the interpretation of peripheral signals to the amygdala and the arcuate nucleus of the hypothalamus, which would stimulate or inhibit food intake.³⁶ Thus, several peptides, such as Peptide YY, pancreatic polypeptide, glucagon-like peptide-1, and oxyntomodulin suppress the desire of feeding,³⁷ whilst ghrelin increases the appetite.^38,39

In the amygdala and the arcuate nucleus (ARC), many neurons co-express neuropeptide Y (NPY) and agouti-related peptide (AgRP), stimulating food intake.⁴⁰ and increasing adiposity. Besides, the brain-derived neurotrophic factor (BDNF), acting in the ventromedial hypothalamus, decreases food intake, antagonizing the NPY neurons.⁴¹ It is expected, therefore, that the degeneration of the BDNF-sensitive neurons may induce obesity.⁴²

In addition, the hypothalamic autophagic pathway⁴³ is essential for the activation of orexigenic and anorectic neurons, controlling appetite in cases of depression, anxiety, panic reactions, and additional noxious stress conditions.^44,45 Impairments also in the central signaling pathways of insulin,⁴⁶ and a decrease in leptin sensitivity are substantial causative factors for obesity^47–50 since insulin and leptin are the main anorectic hormones, activating POMC neurons, which have a high density of leptin receptors.

Intermittent fasting (IF), which is frequently practiced as a popular intervention for the confrontation of obesity^51–54 increases the inflammatory response in the hypothalamus,⁵⁵ a fact that plays a crucial role in the resistance to leptin and insulin activity in the brain. The hypothalamic chronic slow inflammation aggravates the problems of food intake,^56,57 provoking overfeeding and obesity,⁵⁸ with serious psychological effects, which may stimulate furthermore the overfeeding.⁵⁹

The hypothalamic inflammation due to intermitted feeding may be associated with Endoplasmic Reticulum Stress (ER stress),⁶⁰ which may induce changes in neuropeptide gene expression,^61,62 increasing the susceptibility to obesity and insulin resistance.^63,64

Generally, the investigation of obesity at the clinical and experimental level and the application of any efficient therapeutic regime would alleviate the psychosomatic burden of billion of people on earth, ameliorating the quality of life.