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Premier Obesogenic Factors: Overeating and Food Addiction

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Natural Products in Prevention and Therapy of Metabolic Syndrome

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10 February 2023

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14 February 2023

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Abstract
Obesity is characterized by surplus buildup of body lipids primarily in adipose tissue. Prevalence and incidence of obesity are ascending persistently at an alarming rate. Unusual eating behaviors like compulsion to eat (food addiction) and excessive consumption are the premier contributors to obesity. Both are under influence of a variety of stimuli, mainly being stress, emotions, dietary restrictions, sweetness, hyperpalatability, neural pathways, hormonal imbalance and genetics. This review summarizes the potential driving factors behind overeating and food addiction for understanding and exploring obesity linked novel agents and processes as an endeavor to advance treatment approaches. Obesity has been studied extensively throughout the world due to high incidence and association with several metabolic disorders including cardiovascular disorders. The food addition has considered one of potential key factor of obesity and excessive weight gain. Sedentary life style and availability of food also induce obesity.
Keywords: 
Subject: Biology and Life Sciences  -   Endocrinology and Metabolism

Introduction

Obesity is under extensive investigation throughout the world owing to high incidence along with induction of several obesity-associated disorders. Obesity is generally linked with non-homeostatic feeding behavior correlated with overconsumption of food (mainly palatable) for the sake of pleasure rather to fulfill biological requirements. Enhanced caloric intake resulted by failure to control over feeding regardless of knowing the consequences suggested that hyperphagia is a form of food addiction [1]. Out of a wide range of obesogenic factors, the greatest contribution associated with over consumption of energy dense foods due to abnormal eating behaviors [2]. Food addiction (FA) has been emerged as one of the potential key factors of obesity [3].
Food addiction is a chronic and relapsed state characterized by unnecessary consumption of high calorie food in a dysregulated manner. The condition associated with the interactions among different complex fundamental factors that amplify the desire for certain specific dietary items in order to attain the state of excitement, pleasure, energy or to relieve stress [4]. Craving and impulsivity are the main underlying mechanisms of FA. Food craving is a forceful desire to ingest some particular food with minimal resistance [5], while impulsivity is defined as an unintended response to any internal or external stimulus without considering negative impacts [6].
Food addiction has been recognized as fundamental factor in chronic overeating and obesity [7]. With the passage of time human beings are becoming inclined to FA as a result of hedonic system, excessive consumption of food over the requirements [8] mediated by desire and drive neural pathways. Optimum circumstances directing towards food addiction include an abundant supply of energy dense foods, nominal physical exercise and different socio-cultural principles that encourage over ingestion of various products [9,10]. One of the most reliable tools to access food addiction is Yale Food Addiction Scale (YFAS) comprised of 25 measures which are used to evaluate different addictive eating disorders [11].
A study from the field of bariatric surgery has found more than 60% of presurgery patients having histories of grazing like behaviors, exhibiting strong connection with food addiction [12] Some of the most important and potential driving factors behind overeating and food addiction include stress, emotions, neural pathways, dietary restrictions, sweetness, palatability, and genetics.
Stress
Stress being a state of endangered homeostasis triggers diverse behavioral and adaptive responses to stabilize the condition. Stress, weather physiological or environmental in nature, has significant influence on eating behavior. Several studies in animal models have revealed considerable increase in food intake following some stressful condition [13]. Human eating behavior is much similar with animals in sensitivity and response to stress, depending on type and duration of stressor [14]. Meanwhile, lower attraction towards food has been noted in case of some physical harm, illness or fear [15].
Corticotropin-releasing hormone (CRH), norepinephrine and their peripheral factors including pituitary-adrenal axis and divisions of autonomic nervous system, are the premier regulators of stress response. Upon the activation of stress system, multiple behavioral and peripheral changes happen in order to support organism to regulate homeostatic mechanisms [16]. For survival, it is mandatory to cope with stress, an energy consuming process. Multiple processes start in the body including hyperglycemia as a result of glucogenolysis, gluconeogenesis, reduced glucose uptake in tissues; mobilization of amino acids from tissues other than liver, lipolysis and hypermetabolism to enhance available energy [17]. But untreated and recurring stress may lead to serious threats to health and well-being. Repeated exposure to stress stimulates food cravings especially for sweet foods even in the absence of hunger [18].
The hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are the principal effecter pathways of the stress system. According to existing records, chronic stress with mild hypercortisolemia and chronic CNS activation excite fat accumulation in body in addition to eliciting multiple pathologies including diabetes, inflammation and other metabolic syndromes [19]. Higher risk of abdominal fat deposition is seen in case of chronic stress due to HPA axis dysregulation causing continuous over production of glucocorticoids [20]. Glucocorticoids stimulate activity of lipoprotein lipase in adipocytes, thus help in promoting fat storage in adipose tissue [21]. Moreover, they also increase serum insulin, leptin, ghrelin [22] and some hypothalamic neuropeptides [23] stimulate preference for food.
The key endocrine mediator of stress in human is hypothalamic–pituitary–adrenal (HPA) axis with cortisol as end product. Frequent and unmanageable stress stimulates hypercortisolemia by deregulating hypothalamic-pituitary-adrenal axis ultimately influencing food intake behavior and energy homeostasis by inducing glucose intolerance [24] and insulin resistance [14]. Cortisol shows acute as well as chronic effects on metabolism, central nervous system (CNS) and cardiovascular system [25]. Cortisol has shown to be high in about 50% of US population due to their involvement in unhealthy activities including smoking, dietary irregularities and intake of certain medicines like prednisone [26].
Emotions
Emotions play an important part in determining overall human behavior including food choice, liking or disliking of particular food and extent of food consumption. Similarly, mood and feelings of people can also be influenced by the type of food consumed, indicating some intricate relationship between emotions and food intake [27,28]. Both share complex interactions including a number of physiological factors, reward mechanisms, psychological factors, social factors, cultural factors and eating tendencies [29]. Eating in response to emotions, noticeably interrelated with BMI as higher or lower intake of food is parallel with gain or loss of weight respectively [30]. Individuals with high level of emotional eating are at the verge of developing overweight and obesity [31].
Food addiction being similar to drug addiction resulted by strong emotions and ingestion of specific foods, attempt to regulate emotions [32] rather fulfilling their physical requirements [33]. Various investigations have proposed that food choice and consumption are even more affected by emotions rather than profound traditional factors such as liking and desire [34,35]. Furthermore, food choice and eating desire is also associated with positive emotions [36] in addition to negative emotions. But, experiments have revealed a tendency to over consume highly processed foods in food addicts, is attempt to cope with negative emotional state [37,38]. Effects of negative emotions on ingestion behavior are comparatively severe and found greater in females while positive emotions related overeating are found similar in both genders [39].
Negative emotions especially when not regulated properly, guide to overeating [40], prominently in obese rather than normal persons [41]. Negative emotions-triggered hyperphagia coupled with an improvement of mood [42] as elevated level of serotonin was detected in food addicts following energy intake [43]. Hyperphagia in response to anxiety is considered most cited emotion while hyperphagia in response to happiness considered least frequently described form [44]. Emotions associated hyperconsumption suggested to act as mediator between negative emotional status and expected weight gain in female individuals [45]. Healthy as well as eating disordered women demonstrate affinity for overeating due to emotion-oriented handling and disrupted preventive attempts [46]. However, another study has contradicted the idea by revealing overeating as a result of attention and focus for food rather than negative mood [47].
Parental feeding manners and eating restrictions also exert critical impact on children feeding strategies and weight status by directly influencing their emotional eating patterns [48]. Higher caloric intake without hunger by preschool children has been noted while experiencing negative mood whom parents were consuming sweet palatable foods as an attempt to regulate emotions [49]. Stress further ameliorates emotional eating guiding towards building abdominal stores and development of co-morbid medical disorders [50]. Hence, these findings appeal considered emotional management while designing preventive and treatment strategies against obesity [51].
Neural Pathways
Brain reward pathway is one of important circuit related to obesity and addiction. Both share similarity as confirmed by functional brain imaging studies expressing analogous activation patterns of neural pathways when obese and addictive individuals were exposed to certain food or drug of abuse [52,53]. Many other neurological studies have also revealed some shared neural pathways between abnormal food consumption and substance dependence [54,55] by discovering similar hyperactivity in reward related areas and diminished activity in inhibition related areas [56]. Dopamine acts as premier regulator of brain reward circuit. Sufficient concentration of dopamine is released in limbic system [57] and mesolimbic regions following administration of various addictive substances, in humans following exposure to palatable foods [58]. Striatum has also implicated in the regulation of such behaviors revealed by positron emission tomography studies by comparing dopamine D2 receptors between obese and lean individuals [59]. Obese individuals are likely to over consume foods to compensate blunted striatal sensitivity [60]. Brainstem also contributed a greater extent in the regulation of energy homeostasis by receiving neural and hormonal signals from peripheral parts about the nutritional status and adiposity [61].
Currently we are living in an obesogenic environment as highly palatable foods are available everywhere. Exposure to such foods aggravate our desire to consume them, consequently contributing to weight gain [62]. Experimental studies on animals have uncovered same neural mechanisms found in human food addictors after they were allowed a rapid access to sugar, fat and processed food [63,64,65]. Dysregulated food reward mechanism related with the threat for future weight gain especially in case of an unhealthy food environment [66]. Prolonged intake of certain high calorie diets induce molecular and behavioral changes in brain reward centers similar to drugs abuse reinforcing their discriminatory preference [67]. Several neural mechanisms have been implicated in regulation of stimulatory effects of sugar on caloric intake including special peptide systems in hypothalamus like neuropeptides Y and agouti-related protein. Moreover, these appetite stimulant peptides are found effective in inducing fat rich diet intake [68].
Overconsumption of foods affects neural reward pathways, lead to increased salience and seeking for such foods, similar to the processes observed in high alcohol and drug intake [69]. Parallel pattern of activation /inhibition of different brain areas has been noted in obesity and substance addiction, including hyper activation of amygdale, pallidum, putamen, striatum and superior frontal gyrus and inhibition of central operculum and postcentral gyrus [70]. Moreover, excessive activity in amygdala, putamen and thalamus being connected with compulsive eating [71]. Amygdala serves as a meeting point for most important information [72] and it has been extensively investigated for its contribution in emotional processing, fear and anxiety [73]. Based on available evidence important role of amygdala has been proposed towards the development of compelling quest for desirable substance [74]. Besides this, an electroencephalogram study, revealed similar types of brain alterations have been in people with addictive disorders [75].
Desire and appetite pathways work side by side along with hunger pathways [76] and exert potential effects on strength of satiety [77] to access the amount of food consumption for one day, depicting their vital role in eating behavior [78]. The prefrontal cortex is one of the many regions involved in the regulation of eating behaviors by integration with sensory and visceral afferents as well as interacting with hypothalamus and limbic areas through feedback system. In obese people these functional associations altered and control over feeding behavior is lost, leading to unnecessary overeating [79]. It has been observed in recent studies that dietary alterations during gestational period lead to long lasting developmental changes in offspring. A comparative study at embryonic stage has indicated higher expression of different neural substances including hypothalamic orexigenic peptides linked with enhanced stimulation of hypothalamic neuronal precursors and neuroepithelial cells, lead to higher food intake as a consequence of various physiological and behavioral changes [80].
Generally, the central melanocortin system being considered one of the best-characterized neuronal pathways concerned with regulation of energy homeostasis. This complex neuronal network retains the ability to sense stimuli from a range of substance like hormones, nutrients and other neural inputs and regulates long lasting adipostatic signals mainly from insulin and leptin in hypothalamus. Acute regulations are linked with the control of hunger and satiety in the brainstem. Considering the potential regulatory role of these system, serves as a dynamic target for drug developers for treatment of obesity [81].
Dietary Restrictions
Dietary restriction are concerned with intended limitation for food intake and omitting meals even in the presence of hunger [82]. Dieting is a form of energy restriction, related with management of weight loss. Both food restriction and dieting exert their effects on eating habits leads to abnormal eating [83]. In addition to food restriction and dieting, food deprivation also encourages reinforcing value of food [84].
In normal individuals, the food restriction is risk factor for hyperphagia while in the individuals already suffering from some eating disorder, the ongoing illness further prolonged [85]. Experimental studies on laboratory animals have revealed reliable and consistent increase in food intake following food deprivation and food restriction strategies [86]. Although the exact mechanism need to be uncovered, however, food cues and stress may also be underlying factors in this exacerbate eating [38].
Dieting is more often observed in teenage girls as an attempt to improve their appearance resulting nutritional deficiencies and restricted growth [87]. Early age food restrictions are linked with overeating in adolescence thus posing threat for the development of obesity [82]. In addition, maternal restriction can also encourage overeating in early age overweight girls that may be genetically liable to environmental cues [88]. Following a short term restriction of carbohydrates and proteins, participants under observation expressed higher consumption of respective diet [89] indicated dieting individuals experience powerful cravings and difficulty in resistance of foods restriction compared to non-dieters [90]. Desire of sugar consumption continue to ascend as the duration of self-restraint prolongs [91].
Evidence has suggested a history of food restriction and stress promoted abnormal over intake of food even with normal satiation and body weight [92]. Severe and short term energy deficiencies cause modifications in appetite and appetite–regulating hormone concentrations leading to compensatory increase in energy intake thus regaining lost weight in non-obese individuals [93]. Restrained eaters with limited inhibitory control are more likely to failure while attempting to restrict intake, increasing the probability of overeating [94]. Both caloric restriction and overeating have been shown to affect neural processes associated with reinforcement. Both preclinical and some clinical studies have provided evidence that food restriction may increase reward sensitivity similar to drug abuse [95].
Sweetness
Evidence of available knowledge reported that sweet foods encourage appetite, facilitating overeating. Sweet taste exerts its effect through G-protein coupled receptors (T1R2 and T1R3) found in mouth and intestine and secrete different peptides aid in metabolic activities and satiety [96]. Hormonal and metabolic modifications have been noted in individuals taking high glycemic index food, reduces availability of metabolic fuels and stimulate overeating mainly in obese subjects [97]. Energy rich foods are efficient source of daily energy intake and stimulate release of various neuropeptides to elevate mood [98]. Signals for high fat and high sugar diets stimulate food ingestion desire, gradually lead to overeating [99]. Conclusively concentrated sugars rich food and fats act as addictive substances [66].
Carbohydrates, mainly disaccharides like table sugar are considered the most potent addictive dietary substances out of all macronutrients [100]. Sugar encourages the synthesis and release of dopamine in nervous tissue, one of the premier neurotransmitters of addiction pathway [101]. Elevated dopamine secretion has been observed in nucleus accumbens in high sugar fed animals, parallel to the outcome of certain drugs abuse. In addition, a delayed response of acetylcholine neurotransmitter for satiety is noted in such animals [102].
In a series of experimental investigations, role of sugar as an addictive substance has been confirmed owing to similarity of its behavior with well documented effects of addictive drugs [103]. Foods rich in energy, mainly high sugar and high fat diets, are mostly highly palatable in nature. Rewarding mechanisms are the key contributors in sensing these substances more desirable over certain low caloric foods. Resultantly these energy dense highly palatable diets revealed an addictive potential [104]. Inclination towards excessive consumption of hyperpalatable foods with time, specifically sugar rich, fat and salt, associated with their high processing and rapid availability [105].
Different foods have different capacities to induce addiction, based on their processing and composition [106]. Processing along with addition of sweeteners and fats enhances addiction potential of many food items. Although, FA is categorized under both behavioral as well as substance related addiction, however symptoms better fit with later one [56]. An increased level of calmness and reduced levels of anger and tension have been reported after consuming carbohydrate-rich foods. Consumption over long term induces adaptations in the neural reward and stress pathways ultimately encourage depression and opioid-like withdrawal symptoms in case of unavailability of such foods [107,108]. Furthermore, in some animal models anxiety, aggressiveness and teeth chattering has been prominent [103].
Besides the foods, sweetened soft drinks also highly contributed in the pathogenesis of overweight and obesity [109,110]. In a recent meta-analysis, a strong relation between soft drink utilization and higher energy consumption has been proposed [111]. The primary ingredient of these soft drinks is high fructose corn syrup, an important contributor of obesity, due to its sweetness, cheapness and wide availability [112]. Taking sugar sweetened beverages (drinks with added sugars, excluding milk and pure fruit juices) are coupled with surplus caloric intake and higher obesity prevalence due to their little role in regulation of satiety mechanism [113]. A clinical examination has reported that alcoholic beverages are more potent in stimulating total energy intake as compared to soft drinks. In addition, over use of alcoholic beverages at a meal induces thirst owing their diuretic properties [114].
Hyper-palatability
Energy density of a food largely depends on amount of fat in it. High fat foods modify the satiety mechanism [115] and insist an uncontrolled eating drive [116]. Obese people are more prone to overfeeding [117] as claimed by Liu and his colleagues after noticing a delay in satiety signal in obese individuals using functional magnetic resonance imaging technique [118]. Energy efficient diets containing either high proportion of sugars or fats are usually highly palatable in nature. Such diets provoke more portrait for their ingestion by affecting brain reward circuits in comparison to low calorie foods, progressing towards addiction behavior [104]. Chronic over intake of hyperpalatable diets has also stimulated by their high processing and rapid availability [105].
Some palatable and energy efficient foods are consumed as snacks and desserts, contributed obesity development because of continuous intake stimulated by their appetizing nature and their ability to reduce sensitivity of satiety mechanism [119]. Higher salivary secretions have been reported in restrained objects as exposed to sight and smell of palatable foods [120]. Even hyperpalatable foods revealed many dissimilarities with traditional drugs of abuse but still share some of the important features [105]. Utilization both of substances are associated disorderly overuse despite knowing the potential side effects. Consequently, individual fails to control over intake and unable to cut down the consumption [55].
High fat diets act in similar way to enhance sensitization of reward pathways as addiction drugs, rising search for hyperpalatable foods and addictive substances, resulting their overconsumption [32]. Induction for over consumption of hyperpalatable foods has been attributed to hypothalamic neuropeptides mainly being neuropeptide Y (NPY), melanin-concentrating hormone (MCH), agouti-related protein (AgRP), orexin, ghrelin and dynorphin [121]. Food reward, instead of hunger has become central motivational factor for eating today. Even being aware of the potential negative consequences, people consume highly palatable foods, generally rewarding and dense in energy, to seek pleasure. Such foods exhibit numerous similarities to drug cravings observed in both obese and lean drug addicts [122].
Summarizing both historic and current perspectives, a number of processed palatable items express addictive properties analogous to drugs such as nicotine, alcohol, and other neural stimulant [123]. Brain opioid peptide system within the ventral striatum has observed to play important role in regulating responses to highly palatable energy dense foods as confirmed by over intake of palatable foods following stimulation of opioid receptors [124]. Why sweet and palatable foods are difficult to resist? could be answered by sensory properties of sugars and fats. These foods have an uncontrollable sensory appeal that might be natural or learned. Fats impart characteristic texture, flavor and aroma to many foods making them highly palatable. Olfactory perception of volatile fat-soluble molecules is involved in driving towards hyperphagia [125].
Genetics
Along with a number of other important factors, genetics also play major role in energy homeostasis by contributing in maintenance of body energy stores and caloric intake. Genetic mutations can lead to uncontrolled food intake stimulating excess fat deposition ultimately derived to obesity [126]. Using modern technological approaches more than 20 obesity linked genes, primarily active in central nervous system and adipose tissue, have been discovered [127]. The most widely adopted method to investigate role of eating tendencies associated genes comprised of sequencing twins and comparing them with singletons. High palatability, availability and cheapness of food items further support food consumption in genetically susceptible individuals [128]. With the passage of time our genome has evolved according to our lifestyle and environmental conditions in order to ensure our sustainability. In ancient times, physical activity was high with hard availability of food, contrary to the present scenario where food is abundant but expenditure is less, thus storing extra energy in different body tissues [129].
Pro-opiomelanocortin (POMC) secrets many anorexigenic peptides, including melanocyte stimulating hormone (MSH) controls food intake and influences hair color. Mutations in the synthesis and processing of human POMC gene alter the synthesis of MSH and ACTH. Insufficient production of MSH fails to regulate eating behavior as well as hair pigmentation [130] while hypocortisolemia developed by ACTH deficiency drives towards severe and early onset of obesity in response to hyperphagia [131]. Function of POMC in the central melanocortin pathways and energy regulatory processes has been confirmed by studying transgenic animals with loss of POMC gene [132].
Neuropeptide Y (NPY) is attributed as one of the effective orexigenic peptide. Fine and continuous abnormalities imposed by various environmental and genetic factors in complex NPY network stimulates hyperphagia and unusual rate of weight gain results obesity and other relevant metabolic disorders [133]. Even a single intracerebroventricular injection of NPY showed significantly increased feeding in rats [134]. Similarly repeated exposure of this injection for a many days resulted an over consumption of food, increased body weight and higher body fat deposition [135] by stimulating de novo synthesis of fatty acids and triglycerides. Chronic NPY administration has also been associated with abnormal production of glucocorticoids, which in turn induce hyper secretions of insulin and triglycerides. These effects enhance insulin dependent transport of glucose in adipocytes and inhibit transport to muscles, building up of fat stores consequently [136,137,138].
Leptin is one of the major regulators of metabolic pathways conveying information to brain about chronic energy reserves. Primary production site of leptin is adipose tissue and directly proportional to body fat stores. Leptin acts primarily on hypothalamus elicit a series of neuroendocrine reactions that inhibit orexigenic peptides and augment anorexigenic peptides activity [139]. Mutations in Leptin (LEP) and leptin receptor (LEPR) genes are linked with overeating, early-onset obesity and associated phenotypic traits. Additionally, also found responsible for compromised immune system and reproductive capabilities due to diminished production of immune cells and pituitary gonadotropins respectively [140]. Leptin receptors are exclusively found in both NPY and POMC neural populations regulating both in a reciprocal manner. Diminished synthesis of leptin has been linked with lower expression of POMC mRNA and higher expression of NPY mRNA [2]. A point mutation in mice LEP gene showed lack of leptin production and an early induction of obesity, insulin resistance, overeating, hypothermia and lower energy utilization [141]. Four year administration of human leptin via subcutaneous route resulted sustained benefits against multiple congenital human leptin deficiency associated phenotypic abnormalities [142].
Leptin mediate synthesis of POMC derived melanocortin peptides with lessen caloric consumption and body weight by acting on melanocortin-4 receptor (MC4R) [81,143]. MC4 receptors are linked with management of body weight as confirmed by experimental investigation [144]. Mutant MC4 receptor acts as causative site for severe form of obesity. Partial or complete loss of function of these receptors directly depends on nature and extent of mutation [145]. The idea was further supported by experiments on rats and humans using Setmelanotide, a strong MC4R agonist improved weight loss in diet induced obesity and in obese animals with absolute POMC deficiency [146].
The peroxisomal proliferator activated receptors (PPARs) are ligand-activated transcriptional factors played vital role in cell division, inflammation, energy metabolism [147] and adipocyte differentiation. These receptors belong to nuclear hormone receptor superfamily with highest expression in mammalian adipose tissue. Significantly higher expression of PPAR receptor was examine in- in vitro analysis of differentiation of preadipocytes to adipocytes [148]. Another gene, called as Fat mass and obesity-associated (FTO) is also thought to be responsible for regulation of body fat by regulating the satiety mechanism. Mutation in FTO gene is directly associated with increased BMI exhibited diminished responsiveness to satiety signals and enhanced desire of hyperphagia in a food abundant environment along with multiple eating opportunities [149].
Conclusions
Obesity has been studied extensively throughout the world due to high incidence and association with several metabolic disorders including cardiovascular disorders. The food addition has considered one of potential key factor of obesity and excessive weight gain. Sedentary life style and availability of food also induce obesity. Overconsumption of food intake has been associated with factors such as stress, emotions, dietary restrictions, sweetness, palatability, neural pathways, hormonal imbalances, hunger, satiety and genetics.
Stress mediated variation in hypothalamic–pituitary–adrenal (HPA) axis with cortisol as end product ultimately influence food intake behavior and energy metabolism homeostasis. Irregular negative emotions drive overeating prominently in obese rather than normal individuals and negative emotions-triggered hyperphagia coupled with an improvement of mood. Food restriction and dieting, food deprivation also encourages reinforcement of food. Carbohydrates, mainly disaccharides like table sugar are considered the most potent addictive dietary substances associated with food addiction. Some palatable and energy efficient foods such as snacks and desserts, contributed obesity development owing to continuous intake stimulated by their appetizing nature and ability to reduce sensitivity of satiety mechanism. Prolonged intake of certain high calorie diets induces molecular and behavioral changes in brain reward centers similar to drugs abuse and addiction. Leptin mediate synthesis of POMC derived melanocortin peptides with lessen caloric consumption and body weight by acting on melanocortin-4 receptor (MC4R).
Leptin receptor (LEPR) genes are linked with overeating, early-onset obesity and associated phenotypic traits. Fat mass and obesity-associated (FTO) is also thought to be responsible for regulation of body fat by regulating the satiety mechanism. Future studies are required for uncovering dysregulation in neural and molecular pathways, delineation of potential brain areas involved in regulated of food intake and dysregulation associated obesity.

Author Contributions

MAB wrote the manuscript, searched the literature and wrote the manuscript, MA reviewed and edited the manuscript. All authors have read and approved the final manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

Funding source was not available.

Ethical Statement

This article does not contain any studies with human participants or animals used by any of the authors.

Acknowledgments

All data generated or analyzed was obtained from original papers and review articles cited from Google scholar, Science direct and PubMed.

Conflicts of Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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