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A Review on the Role of Food-Derived Bioactive Molecules and the Microbiota-Gut-Brain Axis in Satiety Regulation.
Pizarroso, NA, Fuciños, P, Gonçalves, C, Pastrana, L, Amado, IR
Nutrients. 2021;(2)
Abstract
Obesity is a chronic disease resulting from an imbalance between energy intake and expenditure. The growing relevance of this metabolic disease lies in its association with other comorbidities. Obesity is a multifaceted disease where intestinal hormones such as cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), and peptide YY (PYY), produced by enteroendocrine cells (EECs), have a pivotal role as signaling systems. Receptors for these hormones have been identified in the gut and different brain regions, highlighting the interconnection between gut and brain in satiation mechanisms. The intestinal microbiota (IM), directly interacting with EECs, can be modulated by the diet by providing specific nutrients that induce environmental changes in the gut ecosystem. Therefore, macronutrients may trigger the microbiota-gut-brain axis (MGBA) through mechanisms including specific nutrient-sensing receptors in EECs, inducing the secretion of specific hormones that lead to decreased appetite or increased energy expenditure. Designing drugs/functional foods based in bioactive compounds exploiting these nutrient-sensing mechanisms may offer an alternative treatment for obesity and/or associated metabolic diseases. Organ-on-a-chip technology represents a suitable approach to model multi-organ communication that can provide a robust platform for studying the potential of these compounds as modulators of the MGBA.
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BABY-LED WEANING, AN OVERVIEW OF THE NEW APPROACH TO FOOD INTRODUCTION: INTEGRATIVE LITERATURE REVIEW.
Gomez, MS, Novaes, APT, Silva, JPD, Guerra, LM, Possobon, RF
Revista paulista de pediatria : orgao oficial da Sociedade de Pediatria de Sao Paulo. 2020;:e2018084
Abstract
OBJECTIVE To analyze the scientific literature on Baby-Led Weaning with an integrative literature review to identify risks and benefits. DATA SOURCE The databases used were: National Library of Medicine (MEDLINE), Latin American and Caribbean Literature in Health Sciences (LILACS - Literatura Latino-Americana e do Caribe em Ciências da Saúde), US National Library of Medicine (PubMed), and Virtual Health Library (BVS - Biblioteca Virtual em Saúde) in December 2017. The inclusion criteria established were publications in English with the descriptor "baby-led weaning" in the heading, abstract, or keywords, classified as original articles, of primary nature, and available online and in full. We excluded review articles, editorials, letters to the editor, critical commentaries, and books on the subject, as well as articles not available in full and duplicates. DATA SUMMARY We identified 106 articles, of which 17 met the selection criteria. The Baby-Led Weaning method was significantly associated with the baby's satiety, the start of complementary feeding, and adequacy of weight gain. On the other hand, choking and the intake of micronutrients were negatively associated, however with no statistical differences. CONCLUSIONS Despite the benefits found, the risks still deserve attention and should be investigated with longitudinal randomized controlled studies to ensure the safety of the method when practiced exclusively.
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Gastrointestinal morbidity in obesity.
Acosta, A, Camilleri, M
Annals of the New York Academy of Sciences. 2014;:42-56
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Abstract
Obesity is a complex disease that results from increased energy intake and decreased energy expenditure. The gastrointestinal system plays a key role in the pathogenesis of obesity and facilitates caloric imbalance. Changes in gastrointestinal hormones and the inhibition of mechanisms that curtail caloric intake result in weight gain. It is not clear if the gastrointestinal role in obesity is a cause or an effect of this disease. Obesity is often associated with type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Obesity is also associated with gastrointestinal disorders, which are more frequent and present earlier than T2DM and CVD. Diseases such as gastroesophageal reflux disease (GERD), cholelithiasis, or nonalcoholic steatohepatitis are directly related to body weight and abdominal adiposity. Our objective is to assess the role of each gastrointestinal organ in obesity and the gastrointestinal morbidity resulting in those organs from the effects of obesity.
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Appetite control and energy balance regulation in the modern world: reward-driven brain overrides repletion signals.
Zheng, H, Lenard, NR, Shin, AC, Berthoud, HR
International journal of obesity (2005). 2009;(Suppl 2):S8-13
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Powerful biological mechanisms evolved to defend adequate nutrient supply and optimal levels of body weight/adiposity. Low levels of leptin indicating food deprivation and depleted fat stores have been identified as the strongest signals to induce adaptive biological actions such as increased energy intake and reduced energy expenditure. In concert with other signals from the gut and metabolically active tissues, low leptin levels trigger powerful activation of multiple peripheral and brain systems to restore energy balance. It is not just neurons in the arcuate nucleus, but many other brain systems involved in finding potential food sources, smelling and tasting food, and learning to maximize rewarding effects of foods, that are affected by low leptin. Food restriction and fat depletion thus lead to a 'hungry' brain, preoccupied with food. By contrast, because of less (adaptive thrifty fuel efficiency) or lost (lack of predators) evolutionary pressure, the upper limits of body weight/adiposity are not as strongly defended by high levels of leptin and other signals. The modern environment is characterized by the increased availability of large amounts of energy-dense foods and increased presence of powerful food cues, together with minimal physical procurement costs and a sedentary lifestyle. Much of these environmental influences affect cortico-limbic brain areas concerned with learning and memory, reward, mood and emotion. Common obesity results when individual predisposition to deal with a restrictive environment, as engraved by genetics, epigenetics and/or early life experience, is confronted with an environment of plenty. Therefore, increased adiposity in prone individuals should be seen as a normal physiological response to a changed environment, not in the pathology of the regulatory system. The first line of defense should ideally lie in modifications to the environment and lifestyle. However, as such modifications will be slow and incomplete, it is equally important to gain better insight into how the brain deals with environmental stimuli and to develop behavioral strategies to better cope with them. Clearly, alternative therapeutic strategies such as drugs and bariatric surgery should also be considered to prevent or treat this debilitating disease. It will be crucial to understand the functional crosstalk between neural systems responding to metabolic and environmental stimuli, i.e. crosstalk between hypothalamic and cortico-limbic circuitry.
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Interaction of satiety and reward response to food stimulation.
James, GA, Gold, MS, Liu, Y
Journal of addictive diseases. 2004;(3):23-37
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Obesity is among the most pressing health issues affecting developed countries. The etiology of obesity remains unclear despite its associated health risks. We propose a framework for obesity modeled upon overeating as a substance dependence disorder arising from a combination of abnormal cognitive and neuroendocrine processes. While significant work in both of these fields has investigated the body's regulation of satiety signals, fewer studies have focused upon the mechanisms by which these two seemingly disparate systems interact. Although emotional states have been shown to mediate reward processing, the implications for hunger mediating reward have not previously been addressed. We review the interaction between central satiety signals and reward responses to food stimuli and discuss the implications of this research for understanding the causes of obesity.