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PubMed2006

The hypothalamus, hormones, and hunger: alterations in human obesity and illness.

Obesity is a major global epidemic, with over 300 million obese people worldwide, and nearly 1 billion overweight adults. Being overweight carries significant health risks, reduced quality of life, and impaired socioeconomic success, with profound consequences for health expenditure. The most successful treatment for obesity is gastric bypass surgery, which acts in part by reducing appetite through alterations in gut hormones. Circulating gut hormones, secreted or suppressed after eating food, act in the brain, particularly the hypothalamus, to alter hunger and fullness. Stomach-derived ghrelin increases food intake even in those with anorexia from chronic illness, while pancreatic polypeptide (PP), intestinal peptide YY 3-36 (PYY), oxyntomodulin, and other hormones reduce food intake and appetite. While obese subjects have appropriate reductions in orexigenic ghrelin, other gut-hormone disturbances may contribute to obesity such as reduced anorexigenic PYY and PP. Prader-Willi syndrome (PWS) arises from the loss of paternally inherited genes on chromosome 15q11-13, leading to life-threatening insatiable hunger and obesity from early childhood, through developmental brain, particularly hypothalamic defects. The study of genetically homogenous causes of abnormal-feeding behavior helps our understanding of appetite regulation. PWS subjects have inappropriately elevated plasma ghrelin for their obesity, at least partly explained by preserved insulin sensitivity. It remains unproven if their hyperghrelinemia or other gut-hormone abnormalities contribute to the hyperphagia in PWS, in addition to brain defects. Postmortem human hypothalamic studies and generation of animal models of PWS can also provide insight into the pathophysiology of abnormal-feeding behavior. Changes in orexigenic NPY and AGRP hypothalamic neurons, or anorexigenic oxytocin neurons have been found in illness and PWS. Functional neuroimaging studies, using PET and fMRI, will also allow us to tease apart the hormonal and brain pathways responsible for controlling human appetite, and their defects in obesity.

Brain Mapping↗
PubMed1999

Phenotypic abnormalities in macrophages from leptin-deficient, obese mice.

Obesity is a complex syndrome that involves defective signaling by a number of different factors that regulate appetite and energy homeostasis. Treatment with exogenous leptin reverses hyperphagia and obesity in ob/ob mice, which have a mutation that causes leptin deficiency, proving the importance of this factor and its receptors in the obesity syndrome. Cells with leptin receptors have been identified outside of the appetite regulatory centers in the brain. Thus leptin has peripheral targets. Because macrophages express signaling-competent leptin receptors, these cells may be altered during chronic leptin deficiency. Consistent with this concept, the present study identifies several phenotypic abnormalities in macrophages from ob/ob mice, including decreased steady-state levels of uncoupling protein-2 mRNA, increased mitochondrial production of superoxide and hydrogen peroxide, constitutive activation of CCAAT enhancer binding protein (C/EBP)-beta, an oxidant-sensitive transcription factor, increased expression of interleukin-6 and cyclooxygenase (COX)-2, two C/EBP-beta target genes, and increased COX-2-dependent production of PGE2. Given the importance of macrophages in the general regulation of inflammation and immunity, these alterations in macrophage function may contribute to obesity-related pathophysiology.

Animals↗
PubMed2001

Transcriptional regulation of the leptin gene promoter in rat GH3 pituitary and C6 glioma cells.

Leptin was originally believed to be an exclusively adipocyte-derived hormone regulating appetite and energy balance. It has recently become apparent that leptin is actively expressed in a number of other tissues including the CNS and pituitary, as well as brain- and pituitary-derived cell lines. However, the factors controlling leptin expression in cells of neuroectodermal origin are unknown. The mouse leptin gene 5'-flanking DNA contains multiple AP-1 and SRF-1 binding sites as well as a consensus CRE site at -491 to -482 bp. In addition, a number of potential PIT1 and Oct-1 binding sites may contribute to leptin gene transcription in pituitary and brain. We have used leptin promoter-luciferase reporter constructs to examine the regulation of the leptin promoter in 3T3-L1 preadipocytes, C6 glioma cells, and GH3 pituitary cells in response to serum and hormonal stimuli. Cells were transiently transfected with reporter constructs containing either the proximal 500 bp of the leptin promoter (-500-luc) or 6000 bp of the leptin gene 5' flanking region (-6000-luc). Functional analysis indicates that the leptin promoter is constitutively active in all 3 cell lines. Transcriptional activity was significantly higher with a -500 to +9 promoter than with a construct containing -6000 to +9 bp of 5' flanking DNA, indicating the presence of repressor elements which may contribute to the tissue-specific regulation of leptin expression. However, qualitatively similar results were observed with both constructs in response to serum and hormonal manipulation. Leptin promoter activity was significantly stimulated by serum in all cell lines, although to varying extents. In contrast, the response of the leptin promoter to insulin, IGF-1 and dibutyryl cAMP was cell-type specific and dependent on the presence or absence of FBS in the culture medium. Insulin, IGF-1 and dibutyryl cAMP each caused an approximately two-fold stimulation of leptin promoter activity in 3T3-L1 cells under serum-free conditions, but had no significant effect in the presence of 10% FBS. In contrast, dibutyryl cAMP markedly stimulated leptin promoter activity (5-8-fold) in C6 or GH3 cells in the presence or absence of FBS, whereas insulin or IGF-1 had minimal effects. These findings support our previous studies on the regulation of leptin steady state mRNA levels in C6 cells and demonstrate tissue-specific differences in the regulation of leptin gene transcription in adipose vs. neuroectodermal tissues.

3T3 Cells↗
PubMed2002

Comparison of oral and gastric administration of sucrose and maltose on gastric emptying rate and appetite.

OBJECTIVES: To investigate mechanisms by which specific sugars affect feeding behaviour. DESIGN: In an initial study, gastric emptying rate and appetite were measured following ingestion of lemon flavoured solutions of sucrose, maltose (2160 kJ, 575 ml) and water control (67 kJ, 575 ml) given in randomised order on separate days to six male volunteers. In a second study, the effects of intragastric infusions of sucrose and maltose on appetite and gastric emptying were compared in six male volunteers. RESULTS: When given orally, both the sucrose and maltose solutions slowed gastric emptying compared with water, however sucrose emptied at a faster rate than maltose. The sucrose preload increased fullness and decreased prospective consumption during the following 3 h compared with maltose and water. When administered intragastrically, the gastric emptying rate of sucrose was again faster than that of maltose but there was no difference in ratings of hunger, fullness or prospective consumption for 3 h following the infusions. CONCLUSIONS: These results show that gastric emptying of sucrose is faster than that of maltose and suggest that gastric emptying rate and hence period of gastric distension is not the predominant factor regulating appetite by these sugars. The differences observed between oral and gastric delivery suggest that oro-sensory and cognitive factors, possibly stimulated by the sweetness of sucrose, were involved in the induction of satiety.

Administration, Oral↗
PubMed1998

The Ob protein (leptin) and the kidney.

Mutation of the Ob gene, which encodes for leptin, or mutation of the leptin receptor leads to obesity in mice. Humans, for the most part, have a positive correlation of leptin with body fat mass suggesting possible defects in leptin effector mechanisms that may contribute to obesity. As patients on hemodialysis have difficulty with appetite, we investigated whether leptin is cleared by the kidney and is elevated in hemodialysis patients. In patients with intact renal function there was a net renal uptake of 12% of circulating leptin, whereas in patients with renal insufficiency there was no renal uptake of leptin. In a separate cohort of 36 patients with end-stage renal disease (ESRD), peripheral leptin levels factored for body mass index was increased by fourfold as compared to a group of healthy controls (N = 338). The leptin receptor exists in a long and short form, with the long form primarily expressed in the hypothalamus but also in the lungs and kidneys of the mouse. Further studies are necessary to clarify the role of leptin in regulating appetite in patients with ESRD and the role of leptin in directly affecting kidney function via its receptors.

Animals↗
PubMed1995

Pyroglutamyl peptidase-II ("thyroliberinase") activity in human serum: influence of weight and thyroid status.

The tripeptide hormone, TRH, is metabolized by three enzymes, the most specific of which is pyroglutamyl peptide hydrolase-II (also termed thyroliberinase), a metalloenzyme present in serum and brain. Because pyroglutamyl peptidase-II activity in rat serum is regulated by thyroid hormone levels, we tested the hypothesis that this activity is similarly altered in humans. We studied serum pyroglutamyl peptidase-II activity in 6 patients with hyperthyroidism, 18 patients with hypothyroidism, and 31 euthyroid, normal weight volunteers. Because TRH [or its metabolite cyclo(His-Pro)] is believed to be an important hormone regulating appetite and metabolism, we also evaluated pyroglutamyl peptidase-II activity in 27 euthyroid patients with obesity. Serum pyroglutamyl peptidase-II activity was elevated in patients with hypothyroidism (mean +/- SEM, 33.9 +/- 3.7 nmol/mL.h) compared to that in euthyroid, normal weight volunteers (24.5 +/- 2.8 nmol/mL.h; P < 0.05), but not that in patients with hyperthyroidism (28.3 +/- 4.1 nmol/mL.h; P = NS). Euthyroid obese patients had the highest pyroglutamyl peptidase-II activity (43.6 +/- 2.8 nmol/mL.h; P < 0.0001 vs. normal weight volunteers). Pyroglutamyl peptidase-II activity was positively correlated with body mass index (r2 = 0.30; P < 0.0001). After correction for body mass index, there were no difference in pyroglutamyl peptidase-II activity in hypothyroid, hyperthyroid, and euthyroid individuals. We conclude that serum pyroglutamyl peptidase-II activity is regulated by, or regulates, body weight.

Adult↗
PubMed1996

Effect of cyproheptadine hydrochloride on ingestive behaviors.

Cyproheptadine (CY) has been used therapeutically as an appetite stimulant at a dose which appears to have antiserotoninergic activity. However, the role which CY may play in appetite regulation remains unclear. This study was designed to examine the effect of CY on ingestive behaviours in female Wistar rats. CY administered orally (0.52 mg kg-1 b.w., dissolved in the daily water) for up to six oestrus cycles did not affect 24 h food intake. On the other hand, CY reduced both 24 h liquid intake and 24 h urine output. Furthermore, 24 h liquid consumption and 24 h urine output, were found to fluctuate according to the oestrus cycle.

Animals↗
PubMed2005

Serotonin (5-HT) drugs: effects on appetite expression and use for the treatment of obesity.

The pivotal role of 5-HT in the control of appetite was formally proposed nearly 30 years ago. In particular endogenous hypothalamic 5-HT has been implicated in the processes of within meal satiation and the end state of post meal satiety. Of the numerous 5-HT receptor subtypes currently identified, 5-HT(1B) and 5-HT(2C) receptors are believed to mediate the 5-HT induced satiety. 5-HT drugs such as d-fenfluramine, selective serotoninergic reuptake inhibitor (SSRIs) and 5-HT(2C) receptor agonists have all been shown to significantly attenuate rodent body weight gain, an effect strongly associated with marked hypophagia. D-Fenfluramine, sibutramine, fluoxetine and the 5-HT(2C) receptor agonist mCPP have also all been shown to reduce caloric intake by modifying appetite in both lean and obese humans. Specifically, 5-HT drugs reduce appetite prior to and after the consumption of fixed caloric loads, and reduce pre meal appetite and caloric intake at ad libitum meals. Clinically significant weight loss over a year or more can be produced by both d-fenfluramine and sibutramine treatment, but apparently not by the SSRI fluoxetine. Treatment with the preferential 5-HT(2C) receptor agonist mCPP and the serotonin precursor 5-HTP has also been shown to produce weight loss in the obese. Issues around the actual and possible side effects of these compounds, and in the case of d-fenfluramine toxicity, have led to a search for drugs that act selectively on the CNS 5-HT receptors critical to the satiety response. Currently, a new generation of 5-HT(2C) selective agonists have been developed (including Ro 60-0175, Org 12962, VER-3323, BVT-933 and YM348) and at least one, ADP356, is currently undergoing clinical trials. Hopefully, such drugs will be as or even more effective at regulating appetite and controlling body weight, and will also be free of their predecessors' side effect.

Animals↗
PubMed2006

Biologic clocks and the gut.

The gastrointestinal tract displays biologic rhythms in basal gastric acid output, epithelial cell proliferation, gastrointestinal motility, and appetite regulation. Furthermore, the development of gastrointestinal complications after administration of aspirin and after chemo- and radiotherapy for metastatic colon cancer depends on the time of administration. Biologic rhythms are driven by so-called clock genes. Thus, it is conceivable that subsets of genes in the gastrointestinal tract are under clock gene control as well. The purpose of this article is to discuss basic concepts in the studies of biologic rhythms, to review examples of biologic rhythms in the gastrointestinal tract, and to discuss examples of gastrointestinal diseases in which alterations in biologic rhythms may play a pathogenetic role.

Animals↗
PubMed1991

Neuropeptide regulation of feeding in dogs.

Norepinephrine and four families of neuropeptides, namely, neuropeptide Y (NPY), opioid peptides, galanin, and growth hormone-releasing factor (GRH), have been shown to stimulate feeding after central administration. Because these studies were mainly done on laboratory rats, the present study was designed to ascertain the central stimulators of feeding in dogs. We have shown that porcine and human pancreatic polypeptides (PPs), when administered into the third cerebral ventricle (intracerebroventricularly), increased food and water intake of satiated animals but that the COOH-terminal fragments [hPP-(18-36) and hPP-(23-36)] did not do so at the same molar dose (11.9 nmol). The kappa-opioid receptor agonist dynorphin (A-(1-17) also stimulated food and water intake, whereas alpha-neoendorphin and Met-enkephalin did not. These results suggest the structural specificity of PPs and dynorphin peptides for stimulating feeding. Surprisingly, neither intracerebroventricular injections of NPY and peptide YY nor intracerebroventricular pretreatment with anti-hNPY gamma-globulin modulated feeding, stressing the species differences in the feeding response to exogenous substances and the underlying physiology. Intracerebroventricular injections of norepinephrine, GRH, galanin, and pancreastatin also failed to increase food intake, although most substances tended to or did increase water intake. These results suggest that neuropeptides play a role in a species-specific way in modulating appetite regulation.

Animals↗
PubMed2004

Endocrine and metabolic aspects of adult Prader-Willi syndrome with special emphasis on the effect of growth hormone treatment.

Prader-Willi syndrome (PWS) is a genetic disorder characterized by mild mental retardation, short stature, abnormal body composition, muscular hypotonia and distinctive behavioural features. Excessive eating causes progressive obesity with increased cardiovascular morbidity and mortality. In the PWS genotype loss of one or more normally active paternal genes in region q11-13 on chromosome 15 is seen. It is supposed that the genetic alteration leads to dysfunction of several hypothalamic centres and growth hormone (GH) deficiency (GHD) is common. PWS is well described in children, in whom GH treatment improves body composition, linear growth, physical strength and agility. Few studies have focused on adults. We examined a cohort of 19 young adults with clinical PWS (13 with positive genotype) and mean BMI of 35 kg/m2. At baseline the activity of the GH-insulin-like growth factor-I (IGF-I) system was impaired with low GH values, low total IGF-I and in relation to the obesity low levels of free IGF-I and non-suppressed IGF-binding-protein-1 (IGFBP-1). 2/3 were hypogonadal. Bone mineral density (BMD) was low. Four patients had impaired glucose tolerance and nine patients high homeostasis model assessment (HOMA) index, indicating insulin resistance. Seven patients had a moderate dyslipidemia. The 13 patients with the PWS genotype were shorter and had significantly lower IGF-I. Seventeen (9 men and 8 women), subsequently completed a 12 months GH treatment trial, and GH had beneficial effects on body composition without significant adverse effects. The effects were more pronounced in the patients with the PWS genotype. Analysis of peptides involved in appetite regulation showed that leptin levels were high reflecting obesity and as a consequence NPY levels were low. In relation to the patients obesity circulating oxytocin levels were abnormally low and ghrelin levels abnormally high. Thus, oxytocin and ghrelin might be involved in the hyperphagia. NPY, leptin and ghrelin did not change during GH treatment. In conclusion this pilot study showed that adults with PWS have a partial GH deficiency, and GH treatment has beneficial effects on body composition in adult PWS without significant side-effects. Larger and longer term studies on the effect of GH replacement in adult PWS are encouraged.

Adolescent↗
PubMed1982

Peripherally administered somatostatin reduces feeding by a vagal mediated mechanism.

Somatostatin (SS) is considered to be an important regulator of nutrient homeostasis. As such, we felt it would be of use to study in detail its effects on feeding. Intraperitoneal administration of SS (10 microgram/kg) reduces spontaneous nocturnal feeding (3.6 +/- 0.6 g/2 hr vs 1.6 +/- 0.5 g/2 hr, p less than 0.025). In a separate study we found that SS also reduced spontaneous feeding in sham operated animals, but not in vagotomized animals (1.2 +/- 0.7 g/2 hr vs 3.8 +/- g/2 hr, p less than 0.05). SS inhibited stress (tail-pinch) induced eating at 10 and 1, but not 0.1 microgram/kg and also inhibited insulin (10 U/kg) failed to suppress water intake or ingestion of a 2% sucrose solution suggesting that somatostatin does not suppress feeding by a generalized disruption of behavior or due to the aversiveness of SS. However, food intake also was not suppressed following food deprivation, suggesting a possible aversive effect of SS. We conclude that somatostatin may play a role as one of the physiological signals involved in short-term appetite regulation. Like CCK, the effects of SS would appear to be mediated through the vagus.

Animals↗
PubMed2005

Non-sleep effects of hypocretin/orexin.

Although a role for hypocretin/orexin (HCT/ORX) in sleep/wakefulness and arousal is widely recognized, other actions, not necessarily related to sleep, have been identified. Neurons producing the peptides project to brain sites known to be important in neuroendocrine and autonomic function, as well as appetite regulation. There is consensus that HCT/ORX plays a role in the regulation of cardiovascular function via its effects on sympathetic nervous activity, and the reported pharmacologic effects have been demonstrated to be physiologically relevant. Equally provocative are the actions of these peptides in the hypothalamus and pituitary gland to regulate reproductive and stress hormone secretion. While HCT/ORX are less potent stimulators of food intake than other hypothalamic peptides, HCT/ORX may play an integral role in the organization of hunger and satiation behaviors because of their interaction with those other peptides. In fact recent discoveries of interactions of HCT/ORX with peptides such as corticotropin releasing hormone and neuropeptide Y, as well as with aminergic neurotransmitter systems, are now defining the cellular and molecular mechanisms by which these potent neuropeptides act and promise insight into their physiologic relevance in a variety of non-sleep related behaviors and other homeostatic mechanisms.

Adrenocorticotropic Hormone↗
PubMed2001

The distribution of neuropeptide Y gene expression in the chicken brain.

Neuropeptide Y (NPY) is demonstrated to play an important role in central control of voluntary feed intake (FI) of a variety of species. The commercial broiler chicken has been intensively selected over generations for increased body weight, achieved largely through increased FI. This has resulted in a contemporary animal that does not regulate FI to maintain energy balance, and represents a model for hyperphagia and obesity if allowed unrestricted access to feed. In the present study, the distribution of NPY mRNA was mapped in the brain of juvenile, broiler-strain chicken, and results interpreted in the context of previous data for strains that do not exhibit hyperphagia. NPY mRNA was widely distributed in the broiler brain, and highly expressed in the hippocampus, nucleus commissurae pallii, infundibular hypothalamic nucleus, nucleus pretectalis pars ventralis and neurons around the nucleus rotundus. Moderately labeled neurons were found in the lateral septal organ, nucleus periventricularis hypothalamus and nucleus paraventricularis magnocellularis. The pallium exhibited only sparse labeling. Generally, the distribution of cell groups expressing NPY mRNA was consistent with those regions exhibiting NPY immunoreactivity, and also matches the distribution of receptor binding sites reported in the literature for the chicken brain. This suggests that NPY may be involved in functions controlled by these regions. The observation of NPY gene expression in brain regions involved in appetite regulation is consistent with the recognized importance of NPY in FI regulation in a variety of species, and with the chronic hyperphagia, characteristic of the broiler.

Animals↗
PubMed1982

Primary ketosis in the high-producing dairy cow: clinical and subclinical disorders, treatment, prevention, and outlook.

Bovine ketosis typically occurs in early lactation. Clinical signs include diminished appetite, decreased milk production, loss of weight, hypoglycemia, and hyperketonemia. Susceptibility to ketosis is probably due to the combination of appetite limitation and a high degree of precedence given to the demand of the mammary gland for nutrients, in particular glucose. The precipitating cause is likely to be development of a marked imbalance between glucose supply and glucose requirement. This imbalance then leads to decreased carbohydrate status, decreased insulin secretion, increased fat mobilization, and increased hepatic ketogenesis. Hepatic ketogenesis may be augmented by the diminished carbohydrate status. The role of hormones other than insulin in the etiology of ketosis, although probably important, has not yet been elucidated satisfactorily. Treatment of ketosis involves increasing glucose supply relative to glucose demand. Incidence of clinical ketosis can be minimized by correct nutrition and management as outlined in recommended guidelines. Besides decreasing milk field, clinical ketosis may affect productivity adversely in other ways, for example, by impairing fertility. Subclinical ketosis is important because it may remain undetected and yet have effects on productivity which parallel those elicited by clinical ketosis. Future research should be directed toward understanding mechanisms conferring priority on milk production and regulating appetite.

Acetates↗
PubMed2000

Leptin resistance is associated with hypothalamic leptin receptor mRNA and protein downregulation.

It is well known that leptin plays a predominant role in body weight regulation. Leptin receptors are especially abundant in the hypothalamus, where the majority of leptin's biologic activity occurs. In instances where leptin has no or limited activity, it is easy to implicate leptin resistance and speculate as to the multiple levels where resistance may occur. We hypothesize that leptin resistance is associated with hypothalamic leptin receptor downregulation. Rats were randomly divided into 3 groups receiving phosphate-buffered saline (PBS) or low- or high-dose leptin continually over a 28-day period. Body weight and food intake were measured daily. Long-term leptin treatment resulted in a dose-dependent decrease in body weight for the duration of the study. It also resulted in a dose-dependent decrease in food intake, but only for the first half of the study. A test of leptin resistance was performed at week 3 demonstrating the development of resistance to the anorectic effects of leptin in both treatment groups. The results of the resistance test together with the food intake data suggest that resistance to the appetite-regulating effects of leptin developed during the final 2 weeks of the study. In addition, we show a downregulation of leptin receptor mRNA and protein in the hypothalamus, which may be one of the mechanisms by which the food-intake effects of leptin were lost.

Animals↗
PubMed2002

Pharmacological characterization of cloned chicken neuropeptide Y receptors Y1 and Y5.

The neuropeptide Y (NPY) receptor subtypes Y1 and Y5 are involved in the regulation of feeding and several other physiological functions in mammals. To increase our understanding of the origin and mechanisms of the complex NPY system, we report here the cloning and pharmacological characterization of receptors Y1 and Y5 in the first non-mammal, chicken (Gallus gallus). The receptors display 80-83% and 64-72% amino acid sequence identity, respectively, with their mammalian orthologues. The three endogenous ligands NPY, peptide YY (PYY) and pancreatic polypeptide (PP) have similar affinities as in mammals, i.e. NPY and PYY have subnanomolar affinity for both receptors whereas chicken PP bound with nanomolar affinity to Y5 but not to Y1. A notable difference to mammalian receptor subtypes is that the Y1 antagonist SR120819A does not bind chicken Y1, whereas BIBP3226 does. The Y5 antagonist CGP71863A binds to the chicken Y5 receptor. Anatomically, both Y1 and Y5 have high mRNA expression levels in the infundibular nucleus which is the homologous structure of the hypothalamic arcuate nucleus in mammals. These results suggest that some of the selective Y1 and Y5 antagonists developed in mammals can be used to study appetite regulation in chicken.

Animals↗
PubMed1998

Relationship between hunger-satiety feelings and various metabolic parameters in women with obesity during controlled weight loss.

OBJECTIVE: Satiety plays an important role in weight control. The meaning of fasting hormone levels and satiety feelings, and how post-absorptive changes after meals high in carbohydrate regulate appetite remains to be demonstrated. RESEARCH METHODS AND PROCEDURES: Prospective metabolic study with 25 non-diabetic obese women at the Energy Metabolism Research Unit of the Department of Nutrition Sciences, University of Alabama at Birmingham. We analyzed fasting and postprandial ratings of hunger-satiety and values of various metabolic parameters (serum glucose and insulin, plasma cholecystokinin, respiratory quotient) during controlled weight loss. The postprandial measures were assessed following a test meal providing 320 kcal and yielding a food quotient of 0.89. RESULTS: In the fasting state, there was no correlation between hunger-satiety ratings and any of the measured metabolic parameters. Under postprandial conditions, satiety was positively related to glucose (p=0.002) and insulin (p=0.002) responses to the test meal. In multivariate analysis including glucose, insulin, cholecystokinin, hunger-satiety ratings and respiratory quotient, insulin was the only independent predictor of satiety in the postprandial state. DISCUSSION: These data suggest an association between the endogenous insulin response and feelings of postprandial satiety. Insulin's satiation properties, which could well be mediated by other hormones, may represent a primary factor of food intake regulation after meals relatively high in carbohydrate.

Adult↗