Appetite Control In Humans Research Articles

RD43 rice flour: the effect on starch digestibility and quality of noodles, glycemic response, short-acting satiety hormones and appetite control in humans.

The aim of this study was to develop wheat noodles substituted with 10-40% RD43 rice flour. Starch digestibility and physicochemical and sensory properties of RD43 rice noodles and its effect on glycemic response, gut hormones, and appetite sensation in humans were also determined. The results demonstrated that the substitution of 10-40% RD43 rice flour reduced starch digestibility, the hydrolysis index, and rapidly digestible starch (RDS), while increasing undigestible starch in noodles. Noodles prepared with 30% RD43 rice flour slightly increased water absorption (WA), and the swelling index (SI) without altering cooking loss. When compared with the control, 30% RD43 rice showed higher lightness (L*) and lower redness (a*), yellowness (b*) and hardness with similar overall acceptability. In human studies, ingestion of 30% RD43 rice noodles significantly lowered postprandial plasma glucose at 15-90 min. Interestingly, the postprandial concentration of glucagon-like peptide-1 (GLP-1) and peptide tyrosine-tyrosine (PYY) also significantly increased at 30 min after the intake of 30% RD43 rice noodles. A significantly lower desire to eat and higher fullness were detected after 30% RD43 rice noodle consumption until 120 min. This suggests that RD43 rice flour could be a potential ingredient in noodles for controlling the glycemic response, short-acting satiety hormones, and appetite sensation.

Biomarkers of appetite: is there a potential role for metabolomics?

Knowing the biological signals associated with appetite control is crucial for understanding the regulation of food intake. Biomarkers of appetite have been defined as physiological measures that relate to subjective appetite ratings, measured food intake, or both. Several metabolites including amino acids, lipids and glucose were proposed as key molecules associated with appetite control over 60 years ago, and along with bile acids are all among possible appetite biomarker candidates. Additional metabolites that have been associated with appetite include endocannabinoids, lactate, cortisol and β-hydroxybutyrate. However, although appetite is a complex integrative process, studies often investigated a limited number of markers in isolation. Metabolomics involves the study of small molecules or metabolites present in biological samples such as urine or blood, and may present a powerful approach to further the understanding of appetite control. Using multiple analytical techniques allows the characterisation of molecules, such as carbohydrates, lipids, amino acids, bile acids and fatty acids. Metabolomics has proven successful in identifying markers of consumption of certain foods and biomarkers implicated in several diseases. However, it has been underexploited in appetite control or obesity. The aim of the present narrative review is to: (1) provide an overview of existing metabolites that have been identified in human biofluids and associated with appetite control; and (2) discuss the potential of metabolomics to deepen understanding of appetite control in humans.

Role of hypothalamic tanycytes in nutrient sensing and energy balance.

Animal models are valuable for the study of complex behaviours and physiology such as the control of appetite because genetic, pharmacological and surgical approaches allow the investigation of underlying mechanisms. However, the majority of such studies are carried out in just two species, laboratory mice and rats. These conventional laboratory species have been intensely selected for high growth rate and fecundity, and have a high metabolic rate and short lifespan. These aspects limit their translational relevance for human appetite control. This review will consider the value of studies carried out in a seasonal species, the Siberian hamster, which shows natural photoperiod-regulated annual cycles in appetite, growth and fattening. Such studies reveal that this long-term control is not simply an adjustment of the known hypothalamic neuronal systems that control hunger and satiety in the short term. Long-term cyclicity is probably driven by hypothalamic tanycytes, glial cells that line the ventricular walls of the hypothalamus. These unique cells sense nutrients and metabolic hormones, integrate seasonal signals and effect plasticity of surrounding neural circuits through their function as a stem cell niche in the adult. Studies of glial cell function in the hypothalamus offer new potential for identifying central targets for appetite and body weight control amenable to dietary or pharmacological manipulation.

Current state of the use of neuroimaging techniques to understand and alter appetite control in humans.

It is in the brain where the decision is made what and how much to eat. In the last decades neuroimaging research has contributed extensively to new knowledge about appetite control by revealing the underlying brain processes. Interestingly, there is the fast growing idea of using these methods to develop new treatments for obesity and eating disorders. In this review, we summarize the findings of the importance of the use of neuropharmacology and neuroimaging techniques in understanding and modifying appetite control. Appetite control is a complex interplay between homeostatic, hedonic, and cognitive processes. Administration of the neuropeptides insulin and oxytocin curb food intake and alter brain responses in reward and cognitive control areas. Additionally, these areas can be targeted for neuromodulation or neurofeedback to reduce food cravings and increase self-control to alter food intake. The recent findings reveal the potential of intranasal administration of hormones or modifying appetite control brain networks to reduce food consumption in volunteers with overweight and obesity or individuals with an eating disorder. Although long-term clinical studies are still needed.

Effects of intranasal oxytocin on satiety signaling in people with schizophrenia

Overweight and obesity in schizophrenia are prevalent, affecting half to three-quarters of people with schizophrenia. Hyperphagia and increased meal size have also been implicated as significant contributors to the weight gain problem. Oxytocin has shown to play a role in appetite control in humans and is considered an anorexigenic peptide. This two-day, within-subjects, challenge study involved the examination of satiety after administration of 24 IU oxytocin (intranasal) vs. placebo in participants with a DSM-IV diagnosis of schizophrenia (N = 16). Self reported satiety along with a preload-test meal paradigm were utilized as well as related laboratory measures (insulin, glucose, and leptin), and measures of taste and smell. There were no statistically significant differences between the groups on self-reported satiety or test meal consumption, insulin or glucose levels, or sensory measures. A significant treatment difference was found (F = 5.22, df = 1,97.6, p = 0.025), with a decrease in leptin in the oxytocin group post-administration, but no time effect (F = 1.67, df = 6,95.1, p = 0.180) or treatment by time interaction (F = 1.36. df = 3,4.16, p = 0.261). Despite the small sample and mostly negative findings, we encourage more work to use higher and repeated doses of oxytocin, and to further examine the effect of oxytocin on leptin in schizophrenia as this may be important for understanding both weight control and psychopathology.

The role of meal viscosity and oat β-glucan characteristics in human appetite control: a randomized crossover trial.

BackgroundFoods that enhance satiety can help consumers to resist environmental cues to eat, and improve the nutritional quality of their diets. Viscosity generated by oat β-glucan, influences gastrointestinal mechanisms that mediate satiety. Differences in the source, processing treatments, and interactions with other constituents in the food matrix affect the amount, solubility, molecular weight, and structure of the β-glucan in products, which in turn influences the viscosity. This study examined the effect of two types of oatmeal and an oat-based ready-to-eat breakfast cereal (RTEC) on appetite, and assessed differences in meal viscosity and β-glucan characteristics among the cereals.MethodsForty-eight individuals were enrolled in a randomized crossover trial. Subjects consumed isocaloric breakfast meals containing instant oatmeal (IO), old-fashioned oatmeal (SO) or RTEC in random order at least a week apart. Each breakfast meal contained 218 kcal (150 kcal cereal, and 68 kcal milk) Visual analogue scales measuring appetite were completed before breakfast, and over four hours, following the meal. Starch digestion kinetics, meal viscosities, and β-glucan characteristics for each meal were determined. Appetite responses were analyzed by area under the curve. Mixed models were used to analyze response changes over time.ResultsIO increased fullness (p = 0.04), suppressed desire to eat (p = 0.01) and reduced prospective intake (p < 0.01) more than the RTEC over four hours, and consistently at the 60 minute time-point. SO reduced prospective intake (p = 0.04) more than the RTEC. Hunger scores were not significantly different except that IO reduced hunger more than the RTEC at the 60 minute time-point. IO and SO had higher β-glucan content, molecular weight, gastric viscosity, and larger hydration spheres than the RTEC, and IO had greater viscosity after oral and initial gastric digestion (initial viscosity) than the RTEC.ConclusionIO and SO improved appetite control over four hours compared to RTEC. Initial viscosity of oatmeal may be especially important for reducing appetite.

The role of implicit wanting in relation to explicit liking and wanting for food: Implications for appetite control

Eating is an action open to awareness by the individual; however, it cannot be claimed that processes that control the expression of eating habits are necessarily explicit. This distinction between implicit and explicit processes may enhance understanding of the expression of food reward (particularly the concepts of liking and wanting [Berridge, K. C., & Robinson, T. E. (2003). Parsing reward. Trends in Neurosciences, 26, 507–513] and its importance for human appetite control [Finlayson, G. S., King, N. A., & Blundell, J. E. (2007b). Liking vs. wanting food: Importance for human appetite control and weight regulation. Neuroscience and Biobehavioural Reviews, in press]. The present study investigated the effect of meal-induced satiation on implicit and explicit processes of liking (L) and wanting (W) by developing a computer-based procedure to measure L and W in hungry and satiated states. Explicit measures were derived from analogue ratings whilst an implicit W measure was derived from reaction time in a forced-choice procedure, which also identified food preferences. Seventy subjects (21.8±0.9 years, BMI: 22.2±0.5 kg/m 2) completed the procedure before and immediately following consumption of a savoury test meal. Satiation caused explicit ratings of L and W to decrease in all food categories ( p<0.01); but with a more marked decrease for savoury foods compared with sweet foods ( p<0.01). Implicit W was increased for sweet categories ( p<0.01), but not for savoury. Implicit and explicit measures of L and W independently correlated with preference for sweet foods. This study provides support that implicit and explicit processes of food reward can be simultaneously measured and dissociated using a test meal. Adjustments in hunger were linked to changes in explicit L and W in a manner consistent with sensory specific satiety, while a relationship between hunger and implicit W was absent. We suggest that implicit W is not systematically downregulated by the physiological consequences of food consumption in the same way as hunger and therefore may be largely independent of homoeostatic processes influencing intake.

Low‐dose Pramlintide Reduced Food Intake and Meal Duration in Healthy, Normal‐Weight Subjects

We previously reported that a single preprandial injection (120 microg) of pramlintide, an analog of the beta-cell hormone amylin, reduced ad libitum food intake in obese subjects. To further characterize the meal-related effects of amylin signaling in humans, we studied a lower pramlintide dose (30 microg) in normal-weight subjects. In a randomized, double-blind, placebo-controlled, cross-over study, 15 healthy men (age, 24 +/- 7 years; BMI, 22.2 +/- 1.8 kg/m(2)) underwent a standardized buffet meal test on two occasions. After an overnight fast, subjects received a single subcutaneous injection of pramlintide (30 microg) or placebo, followed immediately by a standardized pre-load meal. After 1 hour, subjects were offered an ad libitum buffet meal, and total caloric intake and meal duration were measured. Compared with placebo, pramlintide reduced total caloric intake (1411 +/- 94 vs. 1190 +/- 117 kcal; Delta, -221 +/- 101 kcal; -14 +/- 9%; p = 0.05) and meal duration (36 +/- 2 vs. 31 +/- 3 minutes; Delta, -5.1 +/- 1.4 minutes; p < 0.005). Visual analog scale profiles of hunger trended lower and fullness higher during the first hour after pramlintide administration. In response to the buffet, hunger and fullness changed to a similar degree after pramlintide and placebo, despite subjects on pramlintide consuming 14% fewer kilocalories. Visual analog scale nausea ratings remained near baseline, without differences between treatments. Plasma peptide YY, cholecystokinin, and ghrelin concentrations did not differ with treatment, whereas glucagon-like peptide-1 concentrations after meals were lower in response to pramlintide than to placebo. These observations add support to the concept that amylin agonism may have a role in human appetite control.

Energy intake/physical activity interactions in the homeostasis of body weight regulation.

The agricultural and technological revolutions of the late 20th century have influenced both of the discretionary components of the energy balance equation, namely energy intake and physical activity. These changes act synergistically in the direction of encouraging weight gain and represent an unprecedented change in man's ecological niche. Obesity is the predictable biologic response to these external changes. This paper reviews the physiologic responses to modern diets and their effect on energy regulation. The energy density of foods is identified as a key element in influencing energy intake due to weak satiety signals that fail to compensate for very energy-dense foods. Evidence is also presented to show that interactions between energy-dense diets and low-levels of physical activity are key elements in encouraging weight gain due to an asymmetry between the hunger and satiety arms of human appetite control.

Fast foods, energy density and obesity: a possible mechanistic link.

Fast foods are frequently linked to the epidemic of obesity, but there has been very little scientific appraisal of a possible causal role. Here we review a series of studies demonstrating that the energy density of foods is a key determinant of energy intake. These studies show that humans have a weak innate ability to recognise foods with a high energy density and to appropriately down-regulate the bulk of food eaten in order to maintain energy balance. This induces so called 'passive over-consumption'. Composition data from leading fast food company websites are then used to illustrate that most fast foods have an extremely high energy density. At some typical outlets the average energy density of the entire menus is approximately 1100 kJ 100 g(-1). This is 65% higher than the average British diet (approximately 670 kJ 100 g(-1)) and more than twice the energy density of recommended healthy diets (approximately 525 kJ 100 g(-1)). It is 145% higher than traditional African diets (approximately 450 kJ 100 g(-1)) that probably represent the levels against which human weight regulatory mechanisms have evolved. We conclude that the high energy densities of many fast foods challenge human appetite control systems with conditions for which they were never designed. Among regular consumers they are likely to result in the accidental consumption of excess energy and hence to promote weight gain and obesity.

Monogenic forms of obesity and diabetes mellitus.

Great progress has been made in identifying several genes and in understanding the molecular pathogenesis of inherited syndromes of obesity and diabetes mellitus (DM). In humans, mutations in leptin, leptin receptor, proopiomelanocortin (POMC), melanocortin-4 receptor (MC4R) and prohormone convertase 1 (PC1) have been described in patients with severe obesity. Most of these obesity disorders, with the exception of the MC4R mutations, exhibit recessive inheritance and a distinct phenotype with varying degrees of hypothalamic dysfunction, and they unravel the critical role of the central leptin and melanocortin pathways in human appetite control and energy homeostasis. Maturity onset diabetes of the young (MODY) is a genetically and clinically heterogeneous subtype of type 2 DM with early onset autosomal dominant inheritance and a primary defect in insulin secretion. To date, six MODY genes have been identified, the glucokinase gene and five beta cell-specific transcription factor genes, hepatocyte nuclear factor-1alpha (HNF-1alpha), HNF-1beta, HNF-4alpha, insulin promoter factor-1 (IPF-1) and NeuroD1/BETA2. Mitochondrial DNA mutations cause another form of DM with an insulin secretory defect that is commonly associated with neurosensory hearing impairment, and has strict maternal inheritance. At the other end of the spectrum are the inherited syndromes of insulin resistance that are caused by mutations in the insulin receptor gene and in the adipocyte-specific transcription factor PPARgamma. The advances in our knowledge of the phenotypic manifestations and underlying molecular mechanisms of genetic syndromes of obesity and DM raise expectations for molecular diagnosis, as well as for more etiological therapies and better prevention of the continuously increasing prevalence of obesity and DM in our modern societies.