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Two times of meal is appreciated by ancient scientists: at the start of the day and before sunset. It is advisable to consume that quantity of food which will be digested within twelve hours, without disturbing daily physical activities. Many efforts have been taken in biomedical science to unlock the complex mechanism underling this appetite science.
 
Two times of meal is appreciated by ancient scientists: at the start of the day and before sunset. It is advisable to consume that quantity of food which will be digested within twelve hours, without disturbing daily physical activities. Many efforts have been taken in biomedical science to unlock the complex mechanism underling this appetite science.
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Proper quantity of food is considered as Sauhitya Matra means eat till the filling of satiety. This satiety term is further differentiated into two functionally different terminologies namely satiation and satiety. Benelam B defines Satiation as the process that leads to termination of eating, accompanied by feeling of satisfaction. This is also called as within meal satiety. Further he defines Satiety as the feeling of fullness that persists after eating, potentially suppressing further energy intake until hunger returns .Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.  
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Proper quantity of food is considered as Sauhitya Matra means eat till the filling of satiety. This satiety term is further differentiated into two functionally different terminologies namely satiation and satiety. Benelam B defines Satiation as the process that leads to termination of eating, accompanied by feeling of satisfaction. This is also called as within meal satiety. Further he defines Satiety as the feeling of fullness that persists after eating, potentially suppressing further energy intake until hunger returns .<ref>Benelam B. Satiation, Satiety and their effects on eating behavior. Nutrition Bulletin. London UK. British Nutrition Foundation. May 2009;34(2):126–173.
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https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1467-3010.2009.01753.x
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</ref>Sorensen LB termed it as between-meal satiety. It is the state where eating is inhibited till next eating episode.<ref>Sørensen LB, Møller P, Flint A, Martens M, Raben A. Effect of sensory perception of foods on appetite and food intake: a review of studies on humans. Int J Obes Relat Metab Disord. 2003;27(10):1152-1166. doi:10.1038/sj.ijo.0802391</ref>
    
Complex network of signals has been involved in development of satiation and satiety. Satiation and satiety involves mechanism which exert their effect through physiological and/or psychological processes. Satiation can modulate the size of meals consumed, controls how much to consume. The physiological mechanism, as outlined by Benelam B. has been referred along with current knowledge which will help to explicit the concept and support to develop objective parameters to asses proper quantity of food (Ahara Matra) –
 
Complex network of signals has been involved in development of satiation and satiety. Satiation and satiety involves mechanism which exert their effect through physiological and/or psychological processes. Satiation can modulate the size of meals consumed, controls how much to consume. The physiological mechanism, as outlined by Benelam B. has been referred along with current knowledge which will help to explicit the concept and support to develop objective parameters to asses proper quantity of food (Ahara Matra) –
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1. '''Sensory and cognitive factors''' :
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1.'''Sensory and cognitive factors''' :
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Sensory and cognitive factors affect intake of food predominantly. Foods sensory properties like taste, smell, texture, appearance, and food type to be consumed affect satiation in the initial period. These sensory specific properties of food are linked with the sensory specific satiety. Sorensen LB et al have reviewed the multiple aspects related to sensory perception of food and their role in appetite regulation. Sensory-specific satiety has an important influence on the amount of food eaten. Palatability of food greatly influences appetite and food intake. Increase in food variety observed rise in quantity of food and energy intake. This study also reviewed standard procedure to test sensory-specific satiety and identified flavor, texture and appearance-specific satieties.  
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Sensory and cognitive factors affect intake of food predominantly. Foods sensory properties like taste, smell, texture, appearance, and food type to be consumed affect satiation in the initial period. These sensory specific properties of food are linked with the sensory specific satiety. Sorensen LB et al have reviewed the multiple aspects related to sensory perception of food and their role in appetite regulation. Sensory-specific satiety has an important influence on the amount of food eaten. Palatability of food greatly influences appetite and food intake. Increase in food variety observed rise in quantity of food and energy intake. This study also reviewed standard procedure to test sensory-specific satiety and identified flavor, texture and appearance-specific satieties.  
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Variety in food and pleasantness of food to sensory organs increase the intake of food. De Graaf C et al concluded that pleasantness of food affect satiation but do not have significant effect on satiety   . The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food   . Study of Spetter M S et al shows that oral food ingestion evokes greater neural activation of brain signaling pathways specifically in the midbrain, amygdala, hypothalamus, and hippocampus area neural activity related to sensory-specific satiety.
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Variety in food and pleasantness of food to sensory organs increase the intake of food. De Graaf C et al concluded that pleasantness of food affect satiation but do not have significant effect on satiety. <ref>De Graaf C, De Jong LS, Lambers AC. Palatability affects satiation but not satiety. Physiol Behav. 1999;66(4):681-688. doi:10.1016/s0031-9384(98)00335-7 </ref>, <ref>Raynor HA, Epstein LH. Dietary variety, energy regulation, and obesity. Psychol Bull. 2001;127(3):325-341. doi:10.1037/0033-2909.127.3.325 </ref>
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The sensory-specific satiety phenomenon has been explained by Rolls et al with reference to sight and test of food.<ref>Rolls ET, Rolls BJ, Rowe EA. Sensory-specific and motivation-specific satiety for the sight and taste of food and water in man. Physiol Behav. 1983;30(2):185-192. doi:10.1016/0031-9384(83)90003-3</ref>, <ref>Rolls BJ, Van Duijvenvoorde PM, Rolls ET. Pleasantness changes and food intake in a varied four-course meal. Appetite. 1984;5(4):337-348. doi:10.1016/s0195-6663(84)80006-9</ref>. Study of Spetter M S et al shows that oral food ingestion evokes greater neural activation of brain signaling pathways specifically in the midbrain, amygdala, hypothalamus, and hippocampus area neural activity related to sensory-specific satiety.<ref>Spetter M S,  de Graaf C,  Mars M, Viergever MA,  Smeets PAM . The sum of its parts—effects of gastric distention, nutrient content and sensory stimulation on brain activation. PLoS ONE. 2014; 9(3): e90872: doi:10.1371/journal.pone.0090872 https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0090872</ref>
    
2. '''Gastric mechanism of satiation:'''
 
2. '''Gastric mechanism of satiation:'''
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a)'''Gastric distention'''- Stomach functions as key component in digestion. It acts as a reservoir of food. The reservoir capacity of the stomach allows it to increase its volume significantly. Its capacity limits the amount of food to be ingested. Stomach distention significantly controls the food intake and satiety.Geliebter A and team while assessing the changes in gastric capacity of obese patients determined the gastric capacity by oral insertion of a latex gastric balloon method .In other works also this is used as a tool to assess the gastric capacity.
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'''a)''''''Gastric distention'''- Stomach functions as key component in digestion. It acts as a reservoir of food. The reservoir capacity of the stomach allows it to increase its volume significantly. Its capacity limits the amount of food to be ingested. Stomach distention significantly controls the food intake and satiety.<ref>Geliebter A, Hashim SA. Gastric capacity in normal, obese, and bulimic women [published correction appears in Physiol Behav 2002 Mar;75(3):433]. Physiol Behav. 2001;74(4-5):743-746. doi:10.1016/s0031-9384(01)00619-9</ref>,<ref>Geliebter A. Gastric distension and gastric capacity in relation to food intake in humans. Physiol Behav. 1988;44(4-5):665-668. doi:10.1016/0031-9384(88)90333-2</ref> Geliebter A and team while assessing the changes in gastric capacity of obese patients determined the gastric capacity by oral insertion of a latex gastric balloon method.<ref>Geliebter A, Schachter S, Lohmann-Walter C, Feldman H, Hashim SA. Reduced stomach capacity in obese subjects after dieting. Am J Clin Nutr. 1996;63(2):170-173. doi:10.1093/ajcn/63.2.170 </ref>In other works also this is used as a tool to assess the gastric capacity.<ref>Tate CM, Geliebter A. Intragastric Balloon Treatment for Obesity: Review of Recent Studies. Adv Ther 34, 1859–1875 (2017). https://doi.org/10.1007/s12325-017-0562-3</ref>
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'''b)''''''Gastric and Intestinal Signals''' – In response to the food many gut peptides are secreted from enteroendocrine cells, which play essential role in regulating food. Steinert RE et al reveals that along with gastric distention, Gastric and intestinal signals (increased GLP-1 and PYY secretions and reduction in plasma ghrelin secretions) synergies to support satiation.<ref>Steinert RE, Meyer-Gerspach AC, Beglinger C. The role of the stomach in the control of appetite and the secretion of satiation peptides. Am J Physiol Endocrinol Metab. 2012 Mar 15;302(6):E666-73. doi: 10.1152/ajpendo.00457.2011. Epub 2012 Jan 3. PMID: 22215654.
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https://journals.physiology.org/doi/full/10.1152/ajpendo.00457.2011?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org</ref>
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b)'''Gastric and Intestinal Signals''' – In response to the food many gut peptides are secreted from enteroendocrine cells, which play essential role in regulating food. Steinert RE et al reveals that along with gastric distention, Gastric and intestinal signals (increased GLP-1 and PYY secretions and reduction in plasma ghrelin secretions) synergies to support satiation.
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Gut hormones such as cholecystokinin (CCK) and GLP-1, Oxyntomodulin (OXM), Peptide YY, Pancreatic polypeptide (PP) these are the important gut hormones involved in the mechanism of satiation, plays significant role in termination of meal. CCK is considered as potential biomarker for satiation.<ref>Melton PM, Kissileff HR, Pi-Sunyer FX. Cholecystokinin (CCK-8) affects gastric pressure and ratings of hunger and fullness in women. Am J Physiol. 1992;263(2 Pt 2):R452-R456. doi:10.1152/ajpregu.1992.263.2.R452</ref><ref>Shah M, Vella A. Effects of GLP-1 on appetite and weight. Rev Endocr Metab Disord. 2014;15(3):181-187. doi:10.1007/s11154-014-9289-5</ref> Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.<ref>Sam AH, Troke RC, Tan TM, Bewick GA. The role of the gut/brain axis in modulating food intake. Neuropharmacology. 2012;63(1):46-56.doi:10.1016/j.neuropharm.2011.10.008</ref>
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Gut hormones such as cholecystokinin (CCK) and GLP-1, Oxyntomodulin (OXM), Peptide YY, Pancreatic polypeptide (PP) these are the important gut hormones involved in the mechanism of satiation, plays significant role in termination of meal. CCK is considered as potential biomarker for satiation  . Oxyntomodulin (OXM) delays gastric emptying and reduces gastric acid secretion, decrease food intake.  
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Leptin, insulin, and ghrelin act as long term regulators of appetite. These are long-acting adiposity hormones. While studying the role of leptin in prandial patterns, researchers observed that plasma leptin concentrations increase during a spontaneous intermeal interval and decline before the onset of a meal. Leptin works through regulation of hypothalamic feeding circuits. Through negative feedback mechanism leptin reduces food intake and regulates body weight homeostasis. Thus decreased leptin levels observed to stimulate appetite behavior. Leptin has an influential role in meal frequency and observed less responsible to control meal size.<ref>Chapelot D, Aubert R, Marmonier C, Chabert M, Louis-Sylvestre J. An endocrine and metabolic definition of the intermeal interval in humans: evidence for a role of leptin on the prandial pattern through fatty acid disposal. Am J Clin Nutr. 2000 Aug;72(2):421-31. doi: 10.1093/ajcn/72.2.421. PMID: 10919937.https://academic.oup.com/ajcn/article/72/2/421/4729460</ref>
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Leptin, insulin, and ghrelin act as long term regulators of appetite. These are long-acting adiposity hormones. While studying the role of leptin in prandial patterns, researchers observed that plasma leptin concentrations increase during a spontaneous intermeal interval and decline before the onset of a meal. Leptin works through regulation of hypothalamic feeding circuits. Through negative feedback mechanism leptin reduces food intake and regulates body weight homeostasis. Thus decreased leptin levels observed to stimulate appetite behavior. Leptin has an influential role in meal frequency and observed less responsible to control meal size.
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Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake. Ghrelin secreted mainly from the gastric mucosa, its level are at their peak just before a meal, and decreased slowly when food nutrients are travelled into intestine.It acts on hippocampal neurons involved in spatial learning and memory, thus empty stomach passes signal to brain for asking to engage in appetite behavior, filling of hunger.Ghrelin as orexigenic factor promoted food intake and weight gain.Various cognitive components participate in the initiation of eating and in the selection of food. Schmid DA et al research findings suggest that along with stimulation of appetite, Ghrelin affects cognitive functions. They have noted vivid, plastic visualization of preferred meal by study subjects after administration of ghrelin.Peptide YY has a suppressive effect on food intake.PPY rise is observed in post prandial phase and are lowest in fasting state. Peripheral administration of PYY3e36 reduces food intake. PPY have shown effect on intestinal motility, delays gastric emptying.  
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Ghrelin potentially enhances appetite. It is the first hormone which shows stimulating effect on food intake.<ref>Wren AM, Seal LJ, Cohen MA, et al. Ghrelin enhances appetite and increases food intake in humans. J Clin Endocrinol Metab. 2001;86(12):5992. doi:10.1210/jcem.86.12.8111</ref><ref>Kalra SP, Bagnasco M, Otukonyong EE, Dube MG, Kalra PS. Rhythmic, reciprocal ghrelin and leptin signaling: new insight in the development of obesity. Regul Pept. 2003;111(1-3):1-11. doi:10.1016/s0167-0115(02)00305-1</ref> Ghrelin secreted mainly from the gastric mucosa, its level are at their peak just before a meal, and decreased slowly when food nutrients are travelled into intestine.It acts on hippocampal neurons involved in spatial learning and memory, thus empty stomach passes signal to brain for asking to engage in appetite behavior, filling of hunger.Ghrelin as orexigenic factor promoted food intake and weight gain.Various cognitive components participate in the initiation of eating and in the selection of food. Schmid DA et al research findings suggest that along with stimulation of appetite, Ghrelin affects cognitive functions. They have noted vivid, plastic visualization of preferred meal by study subjects after administration of ghrelin.<ref>Schmid DA, Held K, Ising M, Uhr M, Weikel JC, & Steiger A (2005). Ghrelin Stimulates Appetite, Imagination of Food, GH, ACTH, and Cortisol, but does not Affect Leptin in Normal Controls. Neuropsychopharmacology, 30(6), 1187–1192. https://doi.org/10.1038/sj.npp.1300670</ref> Peptide YY has a suppressive effect on food intake.<ref>Jones ES, Nunn N, Chambers AP, Østergaard S, Wulff BS, Luckman SM. Modified Peptide YY Molecule Attenuates the Activity of NPY/AgRP Neurons and Reduces Food Intake in Male Mice. Endocrinology. 2019 Nov 1;160(11):2737-2747. doi: 10.1210/en.2019-00100. PMID: 31074796; PMCID: PMC6806261.</ref>PPY rise is observed in post prandial phase and are lowest in fasting state. Peripheral administration of PYY3e36 reduces food intake. PPY have shown effect on intestinal motility, delays gastric emptying.<ref>Asakawa A, Inui A, Yuzuriha H, Ueno N, Katsuura G, Fujimiya M, Fujino MA, Niijima A, Meguid MM, Kasuga M. Characterization of the effects of pancreatic polypeptide in the regulation of energy balance. Gastroenterology. 2003 May;124(5):1325-36. doi: 10.1016/s0016-5085(03)00216-6. PMID: 12730873.</ref>
    
'''Signaling pathways involved in the mechanism of satiation-'''
 
'''Signaling pathways involved in the mechanism of satiation-'''
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Food is considered the basic necessity for sustenance of life and attain physical stoutness [Cha.Sa.[[Sutra Sthana]] 25/40(1)]. Energy hemostasis depends on food we consume. Hypothalamus and brainstem are mainly involved to maintain the energy levels. The arcuate nucleus (ARC) of hypothalamus plays important role to control intake of food. ARC has orexigenic neurons (appetite stimulating) and anorexigenic neurons (appetite inhibiting). During digestion, food nutrients stimulate G-protein coupled receptor present on enteroendocrine cell, which stimulates release of gut hormone. Gut hormones influences the vagus nerve, hypothalamus and brainstem. Stimulating and inhibitory neurons present in hypothalamus interact with peripheral signals which results in alteration of eating drive. Vagal afferents stimulated by the gut hormone and sensitive to the stomach's mechanical stretch further connect with the nucleus of the brainstem. Brainstem passes neural signals to hypothalamus. Numerous hormonal and neural signals influence ARC nucleus, which projects to a number of regions including hypothalamic paraventricular nucleus where some essential energy regulating pathways arise.  
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Food is considered the basic necessity for sustenance of life and attain physical stoutness [Cha.Sa.[[Sutra Sthana]] 25/40(1)]. Energy hemostasis depends on food we consume.Hypothalamus and brainstem are mainly involved to maintain the energy levels. The arcuate nucleus (ARC) of hypothalamus plays important role to control intake of food. ARC has orexigenic neurons (appetite stimulating) and anorexigenic neurons (appetite inhibiting). During digestion, food nutrients stimulate G-protein coupled receptor present on enteroendocrine cell, which stimulates release of gut hormone. Gut hormones influences the vagus nerve, hypothalamus and brainstem. Stimulating and inhibitory neurons present in hypothalamus interact with peripheral signals which results in alteration of eating drive. Vagal afferents stimulated by the gut hormone and sensitive to the stomach's mechanical stretch further connect with the nucleus of the brainstem. Brainstem passes neural signals to hypothalamus. Numerous hormonal and neural signals influence ARC nucleus, which projects to a number of regions including hypothalamic paraventricular nucleus where some essential energy regulating pathways arise.  
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Gastrointestinal track releases various peptide hormones. Stomach has its hormonal and neural control mechanism. Presence of food nutrients along with distention of stomach release gut hormones such as PPY, GLP-1, and oxyntomodulin (OXM).Theses are mainly responsible for phenomenon of satiation. These peptide, decreases hypothalamic orexigenic signaling and increases anorexigenic signaling. Negative feedback mechanism results due to these peptides also contribute to increase satiety between meals. Effect of these gut hormones in union with CNS effect results in satiation and satiety. The enteroendocrine cells released hormones interact at different brain levels through circulation and or through primary afferent neurons. Along with induction of satiation and meal termination, gut hormones also produce a positive feeling of reward and satisfaction. Nutrient sensors and their signaling to brain are vital to give feeling of satisfaction.
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Gastrointestinal track releases various peptide hormones. Stomach has its hormonal and neural control mechanism. Presence of food nutrients along with distention of stomach release gut hormones such as PPY, GLP-1, and oxyntomodulin (OXM).Theses are mainly responsible for phenomenon of satiation. These peptide, decreases hypothalamic orexigenic signaling and increases anorexigenic signaling. Negative feedback mechanism results due to these peptides also contribute to increase satiety between meals. Effect of these gut hormones in union with CNS effect results in satiation and satiety. The enteroendocrine cells released hormones interact at different brain levels through circulation and or through primary afferent neurons. Along with induction of satiation and meal termination, gut hormones also produce a positive feeling of reward and satisfaction.Nutrient sensors and their signaling to brain are vital to give feeling of satisfaction.<ref>Sam AH, Troke RC, Tan TM, Bewick GA. The role of the gut/brain axis in modulating food intake. Neuropharmacology. 2012 Jul;63(1):46-56. doi: 10.1016/j.neuropharm.2011.10.008. Epub 2011 Oct 21. PMID: 22037149</ref> <ref>Murphy KG, Bloom SR. Gut hormones and the regulation of energy homeostasis. Nature. 2006 Dec 14;444(7121):854-9. doi: 10.1038/nature05484. PMID: 17167473.</ref> <ref>Berthoud HR. Vagal and hormonal gut-brain communication: from satiation to satisfaction. Neurogastroenterol Motil. 2008;20 Suppl 1(0 1):64-72. doi:10.1111/j.1365-2982.2008.01104.</ref>
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D Chapelot has described subjective and objective tools for measuring meal size, microstructure of the meal, meal request and intermeal intervals. A multidimensional approach for assessing satiety is proposed with intensity, duration and intake as main variables . Commings DE et.al have reviewed the interaction of gastric, intestinal, and pancreatic signals in food regulation. They have also discussed the important role of short acting GI factors and long-acting adiposity hormones in food intakeregulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.  
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D Chapelot has described subjective and objective tools for measuring meal size, microstructure of the meal, meal request and intermeal intervals. A multidimensional approach for assessing satiety is proposed with intensity, duration and intake as main variables.<ref>Chapelot D. Quantifying satiation and satiety. In: Blundell JE, Bellisle F, ed. Satiation, Satiety and the Control of Food Intake:Woodhead Publishing Series in Food Science, Technology and Nutrition; 2013:Pages12-39.  https://www.sciencedirect.com/science/book/9780857095435</ref> Commings DE et.al have reviewed the interaction of gastric, intestinal, and pancreatic signals in food regulation. They have also discussed the important role of short acting GI factors and long-acting adiposity hormones in food intakeregulation. Gerry Smith survey indicates that gastric signals are volumetric in nature and intestinal signals are nutritive in nature.<ref>Powley TL, Phillips RJ. Gastric satiation is volumetric, intestinal satiation is nutritive. Physiol Behav. 2004 Aug;82(1):69-74. doi: 10.1016/j.physbeh.2004.04.037. PMID: 15234593.</ref>
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Graaf CD et al have discussed various biomarkers of satiation and satiety and suggest there use as a tool to assess satiating efficiency of foods and energy balance. This study has also explained PET and fMRI techniques and referred many works that used these technologies to measure the brain responses to various stimuli in context of satiation.
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Graaf CD et al have discussed various biomarkers of satiation and satiety and suggest there use as a tool to assess satiating efficiency of foods and energy balance. This study has also explained PET and fMRI techniques and referred many works that used these technologies to measure the brain responses to various stimuli in context of satiation.<ref>de Graaf C, Blom WA, Smeets PA, Stafleu A, Hendriks HF. Biomarkers of satiation and satiety. Am J Clin Nutr. 2004 Jun;79(6):946-61. doi: 10.1093/ajcn/79.6.946. PMID: 15159223.</ref>
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Satiety Cascade- Blundell JE and team developed a satiety cascade, referred as fundamental structure to examine the impact of food on satiation and satiety in future research.  
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Satiety Cascade- Blundell JE and team developed a satiety cascade, referred as fundamental structure to examine the impact of food on satiation and satiety in future research.<ref>Blundell JE, Rogers PJ, Hill AJ. Evaluating the satiating power of foods: Implications for acceptance and consumption. In: Solms J, Booth DA, Pangbourne RM, Raunhardt O, editors. Food Acceptance and Nutrition. Academic Press; London: 1987. pp. 205–219.</ref> <ref>Blundell J, de Graaf C, Hulshof T, et al. Appetite control: methodological aspects of the evaluation of foods. Obes Rev. 2010;11(3):251-270. doi:10.1111/j.1467-789X.2010.00714.</ref>
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The satiety quotient (SQ) - GREEN SM et al developed a satiety quotient (SQ) to assess an eating episode's satiating effect. This is considered as a remarkable contribution in the field in quantifying satiating effects of foods. This quotient relates food intake with the rate of return of motivation to eat post ingestion, which is predictive of energy intake. Thus, for a person, the satiety quotient will vary based on weight, macronutrient composition, and energy density of food.
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The satiety quotient (SQ) - GREEN SM et al developed a satiety quotient (SQ) to assess an eating episode's satiating effect. This is considered as a remarkable contribution in the field in quantifying satiating effects of foods. This quotient relates food intake with the rate of return of motivation to eat post ingestion, which is predictive of energy intake. Thus, for a person, the satiety quotient will vary based on weight, macronutrient composition, and energy density of food.<ref>Green SM, Delargy HJ, Joanes D, Blundell JE. A satiety quotient: a formulation to assess the satiating effect of food. Appetite. 1997 Dec;29(3):291-304. doi: 10.1006/appe.1997.0096. PMID: 9468762. https://doi.org/https://doi.org/10.1006/appe.1997.0096</ref>
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Low satiety phenotype - ‘Low satiety phenotype’ is associated with specific behavioral and metabolic profiles that could explain their susceptibility to overeating. These individuals do not recognize their appetite sensation before and after meal. This is considered as an important step in individualized obesity treatment.  
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Low satiety phenotype - ‘Low satiety phenotype’ is associated with specific behavioral and metabolic profiles that could explain their susceptibility to overeating. These individuals do not recognize their appetite sensation before and after meal. This is considered as an important step in individualized obesity treatment.<ref>DrapeauV, Gallant A.The low satiety phenotype. In: Blundell JE, Bellisle F, ed. Satiation, Satiety and the Control of Food Intake: Woodhead Publishing Series in Food Science, Technology and Nutrition; 2013:Pages 273–297. https://doi.org/10.1533/9780857098719.5.273 </ref>
    
'''Research tools to assess digestive fire (Jathragni)-'''
 
'''Research tools to assess digestive fire (Jathragni)-'''
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