The regulation of appetite

Druce, Maralyn

doi:10.1136/adc.2005.073759

Cited by 91 publications

(75 citation statements)

References 61 publications

(56 reference statements)

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“…This supports the assertion that the physical presence of calories, and specifically calories from fat, in the gastrointestinal tract is important for the perception of hunger and satiety sensations. Importantly, we found a temporal association between the attenuated hunger response when fat was removed from the ingested meal, and the blunted change in gastrointestinal peptides (i.e., GIP, GLP-1, and PYY 3-36 ) known to be associated with alterations in the perception of hunger and satiety (12). However, our data do not allow us to assess whether this relationship is causal.…”

Section: Discussioncontrasting

confidence: 61%

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Knuth¹,

Shrivastava²,

Horowitz³

2009

Journal of Applied Physiology

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Knuth ND, Shrivastava CR, Horowitz JF. Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration. J Appl Physiol 106: 122-129, 2009. First published November 13, 2008 doi:10.1152/japplphysiol.90404.2008.-The primary goal of this study was to determine the acute glycemic and endocrine responses to the reduction of fat content from a meal. On three separate occasions, nine overweight subjects (body mass index ϭ 30 Ϯ 1 kg/m 2 ; 5 men, 4 women) consumed 1) a control meal (ϳ800 kcal; 100 g of carbohydrate, 31 g of fat, and 30 g of protein), 2) a low-fat meal (ϳ530 kcal; 100 g of carbohydrate, 1 g of fat, and 30 g of protein), or 3) a low-fat meal plus lipid infusion [same meal as low-fat meal, but the total energy provided was the same as control (800 kcal), with the "missing" fat (ϳ30 g) provided via an intravenous lipid infusion]. All three meals contained [ 13 C]glucose (3 mg/kg body wt) to assess the bioavailability of ingested glucose. During the 5-h period after each meal, we measured the recovery of [ 13 C]glucose in plasma, plasma glucose, and insulin concentrations. We also measured plasma concentration of the gastrointestinal peptides: glucosedependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and peptide YY 3-36 (PYY3-36). The recovery of the ingested [ 13 C]glucose in the hour after ingestion was greater (P Ͻ 0.05) after the low-fat than after the control meal [area under the curve (AUC): 1,206 Ϯ 252 and 687 Ϯ 161 M ⅐ h, respectively]. However, removing dietary fat from the meal did not affect the plasma concentration of glucose or insulin. Importantly, [ 13 C]glucose recovery was not different during the low-fat and lipid infusion trials (AUC: 1,206 Ϯ 252 and 1,134 Ϯ 247 M ⅐ h, respectively), indicating that the accelerated delivery of exogenous glucose found after removing fat from the meal is due exclusively to the reduction of fat in the gastrointestinal tract. In parallel with these findings, the reduction in fat calories from the meal reduced plasma concentration of GIP, GLP-1, and PYY 3-36. In summary, these data suggest that removing fat from the diet expedited exogenous glucose delivery into the systemic circulation and reduced the concentration of key gastrointestinal peptides, yet maintained plasma glucose concentration at control levels. glucose metabolism; incretins; gastrointestinal peptides; low-fat diet; obesity METABOLIC ALTERATIONS after a single meal (e.g., hyperglycemia, hyperlipidemia) have been found to be important independent risk factors for development of obesity-related diseases (19,31,37). However, the impact of the acute response to meal ingestion often gets little attention. For example, despite the fact that low-fat diets have been advocated for weight loss for decades, surprisingly little is understood about the acute metabolic effects of reducing fat calories from the meals. Findings from studies evaluating the metabolic and endocrine responses to the removal of fat from ...

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Section: Discussioncontrasting

confidence: 61%

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Knuth¹,

Shrivastava²,

Horowitz³

2009

Journal of Applied Physiology

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“…Despite the vast amount of data on the involvement of serotonin in the control of food intake, serotonergic mechanisms are sometimes somewhat neglected when brain mechanisms of satiety are being reviewed [377][378][379]. This could provoke the question about the importance of the serotonergic system in in satiety in comparison to other neural and endocrine factors.…”

Section: Serotonin and Satiety -What Is Next?mentioning

confidence: 99%

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

244

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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“…The dot by the side of Figure 3 is scaled to correspond to approximately 1% of the final cumulative intake. These considerations suggest that any effective regulatory physiological system (without assumptions about the type or level of regulation or specific drivers used in regulation; Stock, 1999;Spiegelman and Flier, 2001;Liu et al, 2003;Druce and Bloom, 2006) must achieve much better results than the small percentages indicated above, if good health is to be maintained. Similar calculations can be made for increments in body weight.…”

Section: Carbohydrates Feeding Behaviour and Energy Balancementioning

confidence: 99%

Physiological aspects of energy metabolism and gastrointestinal effects of carbohydrates

2007

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The energy values of carbohydrates continue to be debated. This is because of the use of different energy systems, for example, combustible, digestible, metabolizable, and so on. Furthermore, ingested macronutrients may not be fully available to tissues, and the tissues themselves may not be able fully to oxidize substrates made available to them. Therefore, for certain carbohydrates, the discrepancies between combustible energy (cEI), digestible energy (DE), metabolizable energy (ME) and net metabolizable energy (NME) may be considerable. Three food energy systems are in use in food tables and for food labelling in different world regions based on selective interpretation of the digestive physiology and metabolism of food carbohydrates. This is clearly unsatisfactory and confusing to the consumer. While it has been suggested that an enormous amount of work would have to be undertaken to change the current ME system into an NME system, the additional changes may not be as great as anticipated. In experimental work, carbohydrate is high in the macronutrient hierarchy of satiation. However, studies of eating behaviour indicate that it does not unconditionally depend on the oxidation of one nutrient, and argue against the operation of a simple carbohydrate oxidation or storage model of feeding behaviour to the exclusion of other macronutrients. The site, rate and extent of carbohydrate digestion in, and absorption from the gut are key to understanding the many roles of carbohydrate, although the concept of digestibility has different meanings. Within the nutrition community, the characteristic patterns of digestion that occur in the small (upper) vs large (lower) bowel are known to impact in contrasting ways on metabolism, while in the discussion of the energy value of foods, digestibility is defined as the proportion of combustible energy that is absorbed over the entire length of the gastrointestinal tract. Carbohydrates that reach the large bowel are fermented to short-chain fatty acids. The exact amounts and types of carbohydrate that reach the caecum are unknown, but are probably between 20 and 40 g/day in countries with 'westernized' diets, whereas they may reach 50 g/day where traditional staples are largely cereal or diets are high in fruit and vegetables. Non-starch polysaccharides clearly affect bowel habit and so, to a lesser extent, does resistant starch. However, the short-chain carbohydrates, which are also found in breast milk, have little if any laxative role, although do effect the balance of the flora. This latter property has led to the term 'prebiotic', which is defined as the capacity to increase selectively the numbers of bifidobacteria and lactobacilli without growth of other genera. This now well-established physiological property has not so far led through to clear health benefits, but current studies are focused on their potential to prevent diarrhoeal illnesses, improve well-being and immunomodulation, particularly in atopic children and on increased calcium absorption.

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The regulation of appetite

Cited by 91 publications

References 61 publications

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Reducing dietary fat from a meal increases the bioavailability of exogenous carbohydrate without altering plasma glucose concentration

Serotonin controlling feeding and satiety

Physiological aspects of energy metabolism and gastrointestinal effects of carbohydrates

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