Which micronutrient can reduce appetite?4 answersL-5-hydroxytryptophan, a synergistic combination with effective amounts of vitamin B6, vitamin C, and rhodalia rosea root, can help reduce appetite by increasing serotonin levels, aiding in weight management. N-nonanoylvanillylamine, used as an agent for reducing appetite and imparting a feeling of fullness, can be beneficial for weight reduction and mood enhancement. Additionally, micronutrient deficiencies, such as vitamin D, vitamin B12, iron, iodine, and zinc, can lead to hidden hunger, affecting health and vigor without causing actual hunger, emphasizing the importance of adequate vitamin and mineral intake to prevent undernutrition and related health issues. Incorporating these micronutrients into daily intake through various food products like health bars, smoothies, and drinks can be a practical approach to support appetite control and overall well-being.
How Trigonelline can suppress the hunger?4 answersTrigonelline, a compound found in plants like fenugreek, exhibits various pharmacological properties. Studies suggest that trigonelline can suppress hunger by inducing browning of white adipocytes, enhancing lipid metabolism, and promoting fatty acid oxidation. Additionally, trigonelline has been shown to inhibit the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor, which plays a crucial role in regulating antioxidant proteins and preventing neuro-inflammation. By modulating these pathways, trigonelline may help in managing stress-induced changes in the body, potentially reducing the urge to eat due to stress-related factors. Therefore, trigonelline's ability to influence lipid catabolism, browning of adipocytes, and stress response pathways collectively contribute to its potential in suppressing hunger.
How the gut microbiota effect the satiety state?4 answersThe gut microbiota has been shown to have an impact on satiety and energy intake. The gut microbiome, consisting of trillions of microorganisms, plays a role in regulating processes such as metabolism, nutrition, and physiology. Gut microbial short-chain fatty acids (SCFAs) have been specifically linked to satiety signaling. The gut-brain axis, a bidirectional communication system between the gut and the brain, influences appetite, feeding, and metabolism. Gut hormones, such as ghrelin, cholecystokinin (CCK), and peptide YY (PYY), are involved in coordinating the digestive process and regulating feeding behavior and energy balance. The gut microbiota can modulate food preference and feeding behavior through interactions with the vagus nerve and brain regions involved in feeding regulation. Alterations in signaling of neurotransmitters and neuropeptides, such as dopamine, brain-derived neurotrophic factor (BDNF), and glucagon-like peptide-1 (GLP-1), are associated with the crosstalk between gut microbes and the nervous system. The gut microbiota also influences food intake through peripheral mechanisms, such as the regulation of gut satiety peptide release, and central mechanisms, such as the modulation of hypothalamic neuroinflammation and reward signaling.
What is the physiology involved in the regulation of satiety?5 answersSatiety is regulated by a complex interplay of physiological mechanisms involving the central nervous system, hormones, and feedback signals from the gastrointestinal tract. The hypothalamus plays a crucial role in regulating sensations of hunger and satiety, with interactions between hormones such as ghrelin and leptin influencing food intake and energy homeostasis. Factors such as genetics, gender, age, nutritional status, gut signals, gut microbiota, and individual behavioral responses to food also contribute to satiety. The efficiency of satiety can be influenced by both internal factors, such as sleep and circadian rhythms, and external factors, including environmental and behavioral factors. Additionally, the composition and structure of food can affect satiety responses, with different food groups eliciting varying levels of satiety. Understanding these physiological mechanisms and factors impacting satiety can aid in the development of strategies to control obesity and promote healthy eating habits.
What are the mechanisms by which carbohydrates affect appetite and satiety?5 answersCarbohydrates (CHO) affect appetite and satiety through various mechanisms. One mechanism is the macronutrient hierarchy, where protein has the highest satiety followed by CHO and fat. Energy density (ED) also plays a role, with low ED foods suppressing hunger. The glycemic index (GI) theory suggests that fast-release CHO can cause spikes and troughs in blood glucose, stimulating hunger. On the other hand, the high-fiber theory proposes that foods with high fiber content suppress hunger. Additionally, the peptide theory suggests that CHO can stimulate the secretion of satiety biomarkers and peptides. Glucose and fructose, two types of monosaccharides, have different effects on appetite and reward processing. Fructose ingestion leads to smaller increases in satiety hormones and can increase food-cue reactivity and motivation for food rewards. Overall, the mechanisms by which carbohydrates affect appetite and satiety involve macronutrient hierarchy, energy density, glycemic index, fiber content, and the specific type of carbohydrate consumed.
How nutrient sensing cells in gut suppress satiety?5 answersNutrient sensing cells in the gut suppress satiety through various mechanisms. The release of anorectic peptide hormones, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), by enteroendocrine L-cells in response to food ingestion promotes satiation and satiety. These hormones have effects such as decreasing gastric emptying, increasing satiation, and reducing food intake. Nutrient sensors in the gut mucosa, including taste receptors, respond to macronutrients and coordinate the release of hormones involved in energy and glucose homeostasis. Dysfunction of these nutrient sensors may contribute to metabolic dysfunctions associated with obesity. Additionally, postoral signaling from the gut to the brain, mediated by vagal and splanchnic afferents, plays a role in the negative feedback control of satiety after nutrient intake. The specific mechanisms underlying the suppression of satiety by nutrient sensing cells in the gut are still being investigated.