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Results for “Appetite Regulation”

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At least 361 records · Page 20Linked to original sources
PubMed1999

Anandamide induces overeating: mediation by central cannabinoid (CB1) receptors.

RATIONALE: Central cannabinoid systems have been implicated in appetite regulation by the respective hyperphagic actions of exogenous cannabinoids, such as delta9-THC, and hypophagic effects of selective cannabinoid receptor antagonists. OBJECTIVE: This study examined whether an endogenous cannabinoid, anandamide, could induce overeating, via a specific action at central (CB1) cannabinoid receptors. METHODS: Pre-satiated male rats (n=18), received subcutaneous injections of anandamide (0.5, 1.0, 5.0, 10.0 mg/kg) before 3-h, nocturnal food intake tests. In a second series of intake tests (n=8), anandamide injection (1.0 mg/kg) was preceded by injection of the specific CB1 receptor antagonist, SR141716 (0.1, 0.5, 1.0 mg/kg SC). RESULTS: All doses of anandamide induced significant overeating, with 1.0 mg/kg being most potent. Additionally, hyperphagia induced by 1.0 mg/kg anandamide was dose-dependently attenuated by SR141716 pretreatment. CONCLUSION: This first demonstration of anandamide-induced, CB -mediated, overeating provides important evidence for the involvement of a central cannabinoid system in the normal control of eating.

Animals↗
PubMed2001

Determination of enterostatin in human cerebrospinal fluid by capillary electrophoresis with laser induced fluorescence detection.

A capillary electrophoresis (CE) method with laser induced fluorescence (LIF) detection is described for quantification of enterostatin (Val-Pro-Asp-Pro-Arg), a pentapeptide involved in appetite regulation and insulin secretion. Enterostatin and two other pentapeptides belonging to the enterostatin family (i.e. Ala-Pro-Gly-Pro-Arg and Val-Pro-Gly-Pro-Arg) were well separated from each other. The peptides were fluorescently tagged with naphthalene-2,3- dicarboxaldehyde (NDA) and separated by micellar electrokinetic chromatography (MEKC) in the presence of methanol as an organic modifier. Coupled with LIF detection, the method had a detection limit of 4.8 x 10(-6) M for enterostatin. The relative standard deviation was to be 4.0% from five determinations of enterostatin at 37.2 microM in a human cerebrospinal fluid (CSF) sample. Twenty-three human CSF samples were analyzed. The level of enterostatin ranged from 24 microM to 51 microM with a mean (+/- SEM) value of 41.7 +/- 2.0 microM.

Amino Acid Sequence↗
PubMed2026

Genetic determinants of obesity: mechanisms, clinical implications, and targeted therapies.

PURPOSE: Obesity is a major global health crisis with rising prevalence in both pediatric and adult populations, leading to an increased risk of cardiovascular, metabolic, and other chronic complications affecting all organ systems. A clear understanding of the genetic contributors to polygenic, syndromic, and monogenic obesity is essential for early diagnosis and targeted management. METHODS: Advances in genome-wide association studies (GWAS) and sequencing technologies have greatly expanded our understanding of the genetic alterations underlying this multifaceted disease and have helped in delivering personalized treatment. RESULTS: The pathogenesis of common, polygenic obesity is related to a complex interplay between genetic susceptibility and environmental factors. Syndromic obesity, a less common form, is characterized by early-onset accompanied by additional features such as developmental delay, dysmorphic traits, and various organ system involvement. The rarest form, monogenic obesity, is characterized by severe early-onset non-syndromic obesity caused by mutations in single genes regulating appetite within the hypothalamus. These monogenic obesity cases, though infrequent, have been instrumental in elucidating key pathways involved in hunger and satiety. CONCLUSION: This review provides a comprehensive summary of the most recent findings on the genetic basis of obesity across all age groups, highlighting clinical implications and emerging therapeutic opportunities.

Humans↗
PubMed1995

A paradoxical elevation of brain cyclo(His-Pro) levels in hyperphagic obese Zucker rats.

Several studies suggest a role for endogenous cyclo(His-Pro) or CHP in appetite regulation. In the present study, we have examined the regional brain distribution of CHP in hyperphagic obese Zucker rats and their lean littermates. The data show a significant elevation in the levels of CHP in many brain regions, including hypothalamus of the obese rat. Within the hypothalamus, the lateral hypothalamic (LH) nucleus of obese rats had significantly higher levels of CHP when compared to that of the lean littermates. Administration of dehydroepiandrosterone, a steroid hormone known to decrease food intake and body weight gain, to obese rats led to decrease in the levels of CHP in the LH. These data further suggest a role for the endogenous CHP in attenuating food intake.

Animals↗
PubMed1984

Antagonism of diazepam-induced feeding in rats by antisera to opioid peptides.

Diazepam-induced feeding in rats is antagonized not only by the opiate antagonist naloxone but also intraventricular administration of specific antisera to the endogenous opioid peptides met-enkephalin or beta-endorphin. Pituitary beta-endorphin is probably not implicated in the diazepam effect since blockade with the glucocorticoid dexamethasone of the release of beta-endorphin from the anterior pituitary does not modify the diazepam-induced feeding, which is however prevented by TRH, a suggested physiological antagonist of some of the effects of opioid peptides. The possible central participation of both beta-endorphin and met-enkephalin in the ingestive behavior induced by diazepam gives further support to the postulated physiological role of endogenous opioids in appetite regulation.

Animals↗
PubMed1993

Altered cerebrospinal fluid amino acid pattern in the anorexia of aging: relationship with biogenic amine metabolism.

To study the possible role of several amino acids on feeding in the anorexia of aging, we have measured plasma and cerebrospinal fluid (CSF) concentrations of 22 amino acids in 14 elderly persons with idiopathic anorexia and 10 healthy subjects with normal weight in a similar age range. Plasma and CSF amino acid concentrations and CSF homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) levels were all measured by HPLC methods. Elderly anorectic subjects had significantly lower levels of glutamic acid but increased concentrations of glutamine in both plasma and CSF compared to controls. Likewise, a significant increase of histidine, threonine, alanine, arginine, valine, methionine, isoleucine, leucine, phenylalanine, tryptophan, ornithine and lysine was found in CSF, but not in plasma, from patients with anorexia. Besides, the CSF histidine/LNAA (large neutral amino acids) and tryptophan/LNAA ratios were elevated in anorectic patients as compared with controls of similar age. In addition, we found higher CSF concentrations of HVA and 5-HIAA, as well as a positive correlation between CSF LNAA and either HVA (r = 0.74, p = 0.002) or 5-HIAA (r = 0.61, p = 0.020) concentrations in elderly anorectics. CSF tryptophan correlated positively with 5-HIAA levels (r = 0.59, p = 0.026) and CSF tyrosine with HVA levels (r = 0.77, p = 0.002). Our results suggest that changes in the CSF concentration of amino acids could contribute to an increased biogenic amine metabolism in the central nervous system of elderly anorectic subjects, possibly increasing the synaptic liberation of biogenic amines involved in the appetite regulation.

Aged↗
PubMed1984

Zinc deficiency and anorexia in rats: normal feeding patterns and stress induced feeding.

We report the effects of zinc deficiency on normal feeding behavior in rats and the effects of zinc deficiency on stress-induced eating in rats. Zinc deficient (ZD) rats weighed significantly less than their pair-fed and ad lib controls. Zinc repletion allowed improved growth, but ZD rats never displayed catch-up growth compared to their ad lib controls. ZD rats rapidly developed a depressed food efficiency ratio which normalized with zinc supplementation. Food consumption in ZD rats was approximately one-third that of ad lib controls and water intake was also significantly reduced. Mild tail pinch was able to induce feeding in these normally anorexic ZD rats. We conclude that zinc deficiency represents an interesting model of anorexia which may enhance our understanding of appetite regulation.

Animals↗
PubMed1986

Effects of manipulations of glucoregulation on feeding in the ground squirrel.

Insulin and 2-deoxy-D-glucose (2-DG) stimulate feeding in rats, while glucagon inhibits feeding. We report here their effects on food intake in the 13-lined ground squirrel (Spermophilus tridecumlinectus). These hibernating animals are an interesting model for studying appetite regulation because of the marked seasonal variations in food consumption. Food intake reached a peak of 286 +/- 7 g/kg/day in mid July, decreasing to 16.1 +/- 3 g/kg/day in September. Studies during the hyperphagic period showed that glucagon (0.5 to 1 mg/kg) decreased feeding 30 minutes post injection (p less than 0.01) whereas at 4 hours glucagon produced a 37% increase in feeding (p less than 0.05). During the hypophagic period, glucagon failed to alter food consumption. Insulin (5-100 Units/kg) produced no effect on feeding in hyperphagic animals despite a decrease in glucose from 193 +/- 10 mg/dl to 55 +/- 4 mg/dl after 100 Units/kg. However, insulin (50 and 100 Units/kg) resulted in significant increases in food consumption at 2 and 4 hours (p less than 0.01 and 0.05, respectively) when administered while the animals were hypophagic. 2-DG (250-750 mg/kg) increased food consumption (hyperphagic phase) by 76% at 20 hours (p less than 0.01) with significant increases being present as early as 4 hours, although when 2-DG was given to hypophagic animals it resulted in decreased food intake at 4 hours (p less than 0.05). We conclude that the effects of glucoregulatory manipulations on food consumption are markedly influenced by the circannual rhythm of feeding in the 13-lined ground squirrel.

Animals↗
PubMed1987

Severe reduction in food intake by pregnant rats resembles a learned food aversion.

To assess the effects of sucrose, low levels of dietary protein, and pregnancy on food intake, sixty-four female rats were assigned to eight groups in a 2 X 2 X 2 design. Food, water, and sucrose intake and rats' weights were measured daily. Pregnant rats offered sucrose with low protein (8%) diets did not maintain adequate weight gain during pregnancy; 25% of these subjects perished during the last days of pregnancy. These results have implications for human populations that have high birth rates and diets that are deficient in protein. A hormonal mechanism which regulates appetite or taste preferences during pregnancy is postulated and a "learned food aversion" interpretation is given for the data.

Animals↗
PubMed1983

Effect of centrally administered neurotensin on multiple feeding paradigms.

Recent studies have suggested that the tridecapeptide, neurotensin, may be an endogenous satiety factor. The present study was undertaken to examine the effects of neurotensin on multiple paradigms known to stimulate feeding. Following a 30 hour starvation period, neurotensin suppressed feeding at the 20 microgram and 10 microgram dose, but not at the 1 microgram dose when compared to saline controls. Norepinephrine (20 micrograms ICV) induced feeding was suppressed at the 20 microgram neurotensin dose but not at the 10 microgram or 1 microgram dose. In contrast, neurotensin did not suppress muscimol induced feeding at any of the doses. Insulin induced feeding (10 units SC) also was not suppressed by neurotensin. Neurotensin suppressed dynorphin induced feeding at the 20 microgram and 10 microgram but not at the 1 microgram dose. Neurotensin suppressed spontaneous feeding (p less than 0.01) in vagotomized rats (2.5 +/- 0.3 g/2 hr) when compared with saline controls (4.2 +/- 0.5 g/2 hr) suggesting that an intact vagus is not necessary for neurotensin's anorectic effect. We conclude that neurotensin may play a role in short-term appetite regulation by a complex interaction with monoamines and neuropeptides, particularly norepinephrine and the kappa opiate agonist, dynorphin.

Animals↗
PubMed1986

Destruction of noradrenergic innervation to the paraventricular nucleus: deficits in food intake, macronutrient selection, and compensatory eating after food deprivation.

Norepinephrine (NE) injected into the paraventricular nucleus (PVN) has a stimulatory effect on feeding behavior and is found to selectively enhance preference for carbohydrate in the rat. The present experiments were conducted to assess the impact of chronic depletion of NE within the PVN on food intake and appetite regulation. The catecholamine (CA) neurotoxin, 6-hydroxydopamine (6-OHDA), when administered into the PVN, produced a significant depletion of PVN NE in association with a variety of behavioral changes. The immediate consequence of the neurotoxin lesion was a dramatic increase in 24-hr food intake, attributed predominantly to a preferential increase in carbohydrate and fat consumption. The long-term effects related to CA depletion were a deficit in daily food consumption, particularly of carbohydrate (-42%). Although animals with diminished PVN NE maintained a normal diurnal feeding pattern, they failed to exhibit the increased ingestion of an energy-rich carbohydrate diet which rats normally show during the dark period of the diurnal cycle. Rats injected with 6-OHDA directly into the PVN exhibited a normal response to glucoprivic challenge, but demonstrated a deficit in their ability to produce compensatory feeding, particularly of carbohydrate and fat, in response to food deprivation. These findings suggest a specific function for PVN noradrenergic mechanisms in normal energy repletion when body energy stores are reduced.

Adaptation, Physiological↗
PubMed1992

Yohimbine attenuates clonidine-induced feeding and macronutrient selection in genetically obese (ob/ob) mice.

Biochemical abnormalities in the hypothalamus of the genetically obese (C57B1/6J, ob/ob) mouse, including increased levels of endogenous norepinephrine (NE) in the paraventricular nucleus (PVN) and reduced medial hypothalamic NE metabolism, have been cited as evidence of a CNS defect contributing to altered caloric intake in this genetic strain. In the current study, the alpha 2-antagonist yohimbine (YOH) and the alpha 2-agonist clonidine (CLON) were administered systemically to 6-h meal-feeding obese and lean mice. Yohimbine (3-5 mg/kg, IP) significantly reduced total energy intake and intake of carbohydrate and fat, in both phenotypes, without altering protein intake. In contrast, CLON (25 micrograms/kg, IP) potentiated feeding, resulting in a shift in macronutrient selection toward a significant increase in the proportional intake of carbohydrate. Obese mice, however, showed an enhanced behavioral response to CLON injection. Pretreatment with 1 mg/kg YOH, a dose that alone did not significantly alter energy intake or diet selection, blocked CLON's stimulatory effect on feeding and carbohydrate preference. These results are consistent with a role for alpha 2-noradrenergic receptors in appetite regulation of ob/ob and lean mice and suggest that disturbances in this system may be involved in the development of genetic obesity.

Animals↗
PubMed1994

Evidence for cholecystokinin receptor subtype in endocrine pancreas.

Cholecystokinin (CCK) is a gut hormone that regulates pancreatic endocrine functions via CCKA receptors. CCK4 (Trp-Met-Asp-Phe-NH2) has an insulinotropic effect, but is 1000-fold less potent than CCK8. The in vitro potencies and selectivity of newly synthesized CCK4 analogs were investigated. Exchanging various a amino acids, for example Met by Nle and modifying Phe and/or Trp, led to compounds that were much more effective than CCK4 itself and show insulinotropic effects comparable with those of CCK8. Compounds that possess electron withdrawing groups on the C-terminal phenylalanine were especially effective; compounds with electron-donating groups had no effect. In contrast to CCK8 the synthetic CCK4 compounds were selective for the endocrine pancreas: they had no agonistic or antagonistic effect on the contraction of the guinea pig ileum, amylase release from isolated acini, and no major effect on the feeding behavior of mice being supplied with either compound by an implantable AlzetR pump for 8 days. The data indicate that some of the synthetic tetrapeptides exhibit a high affinity for the CCK receptor of the endocrine pancreas and that they are highly selective for this (peripheral) CCKA receptor subtype. The beta-cell CCKA receptors are different from those in exocrine pancreas, smooth muscle, and those for regulating appetite; these peripheral receptor subtypes can be discriminated for the first time.

Amylases↗
PubMed1985

Clinical studies with corticotropin releasing factor: implications for the diagnosis and pathophysiology of depression, Cushing's disease, and adrenal insufficiency.

Corticotropin releasing factor (CRF) is a 41 amino acid peptide first isolated from sheep hypothalami and thought to be a principal modulator of the hypothalamic-pituitary-adrenal cortical (HPA) axis. We report herein a series of clinical studies with CRF in healthy volunteers and in patients with abnormalities in HPA function, including depression, Cushing's disease, Cushing's syndrome, and Addison's disease. Our data indicate that CRF can be a diagnostic aid in distinguishing various disorders of the HPA axis from one another, including Cushing's disease from depression and secondary from tertiary adrenal insufficiency. Moreover, the hormone responses to CRF help clarify the pathophysiology of the HPA abnormalities in several disorders. For instance, our data indicate that hypercortisolism in Cushing's disease results principally from a defect at the level of the pituitary; in contrast, in depression the defect seems to be hypothalamic, possibly involving hypersecretion of endogenous CRF. This latter possibility is of particular interest in light of clinical observations that depression often can be precipitated by stress. Moreover, data from experimental animals show that CRF may influence several processes known to be altered in the overall symptom complex of depression, including not only pituitary-adrenal function, but also motor activity, appetite regulation and sexual behavior.

Addison Disease↗
PubMed1994

Longevity effect of chromium picolinate--'rejuvenation' of hypothalamic function?

The first rodent longevity study with the insulin-sensitizing nutrient chromium picolinate has reported a dramatic increase in both median and maximal lifespan. Although the observed moderate reductions in serum glucose imply a decreased rate of tissue glycation reactions, it is unlikely that this alone can account for the substantial impact on lifespan; an effect on central neurohormonal regulation can reasonably be suspected. Recent studies highlight the physiological role of insulin as a modulator of brain function. I postulate that aging is associated with a reduction of effective insulin activity in the brain, and this contributes to age-related alterations of hypothalamic functions that result in an 'older' neurohormonal milieu; consistent with this possibility, diabetes leads to changes of hypothalamic regulation analogous to those seen in normal aging. Conversely, promoting brain insulin activity with chromium picolinate may help to maintain the hypothalamus in a more functionally youthful state; increased hypothalamic catecholamine activity, sensitization of insulin-responsive central mechanisms regulating appetite and thermogenesis, and perhaps trophic effects on brain neurons may play a role in this regard. Since both the pineal gland and thymus are dependent on insulin activity, chromium may aid their function as well. Thus, the longevity effect of chromium picolinate may depend primarily on delay or reversal of various age-related changes in the body's hormonal and neural milieu. A more general strategy of hypothalamic 'rejuvenation' is proposed for extending healthful lifespan.

Aging↗
PubMedDate not supplied

Two satiety systems revealed by hypothalamic knife cuts in hypophysectomized rats.

When pituitaries are intact, hypothalamic knife cuts produce obesity in adult rats but not in weanlings. Knife cut weaning females do not usually begin to become obese until after they are 7 weeks old. When pituitaries are removed, symmetrical or asymmetrical knife cuts produce obesity promptly in both adults and weanlings. Obesity indices that correct for stunted linear growth reveal that in adults the degree of obesity is independent of the presence or absence of the pituitary. Based on these findings we speculate that there may be two appetite regulating systems, a juvenile one involving the pituitary, and an adult one involving the hypothalamus.

Animals↗
PubMed1986

Amphetamine: effects on meal patterns and macronutrient selection.

Catecholaminergic systems, specifically in the region of the lateral perifornical hypothalamus (PFH), have been linked to the inhibition of feeding behavior. The present studies examined the effects of d-amphetamine (AMPH), which is believed to act through the release of endogenous catecholamines (CAs), on spontaneous feeding and appetite regulation in rats. Injection of AMPH directly into the PFH caused a marked suppression of food intake; changes in computer-monitored meal patterns were characterized by an increase in the latency to meal onset and a consequent reduction in meal size and duration. This suggests that hypothalamic AMPH administration may influence primarily the initiation, rather than the termination, of feeding. In other experiments, chronic infusion of AMPH directly into the PFH was shown to suppress 24 hr food intake and body weight gain, indicating the effectiveness of lateral hypothalamic CA stimulation in overriding normal long-term patterns of feeding. The effect of hypothalamic CA stimulation on macronutrient selection was also investigated in groups of rats injected either centrally or peripherally with AMPH, or centrally with the CA agonists, dopamine and epinephrine. Each of these manipulations caused a strong inhibition of protein intake with no effect on carbohydrate, and only a mild suppression of fat ingestion after peripheral AMPH. These selective effects of AMPH on feeding patterns and diet choice, provide support for a role of CA innervation to the lateral hypothalamus in the modulation of natural feeding behavior and macronutrient selection.

Animals↗
PubMed2004

Plasma ghrelin levels are normal in obese patients with idiopathic intracranial hypertension (pseudotumor cerebri).

PURPOSE: Idiopathic intracranial hypertension (IIH) occurs predominantly in young, obese women. Weight loss may alleviate symptoms of IIH yet may be difficult to achieve. Ghrelin, a gastric hormone, is involved in normal body weight and appetite regulation. Its levels are elevated in syndromes of overeating and decline in simple obesity. We postulated that fasting plasma ghrelin levels are elevated in IIH patients and that the typical postprandial decline in plasma ghrelin may not occur. DESIGN: Prospective, observational case-control study. METHODS: Prospective study. SETTING: University hospital and clinic. STUDY POPULATION: Sixty-five patients with a diagnosis of IIH and 25 obese control patients (screened for IIH symptoms). Patients with intracranial abnormalities or a history of gastric surgery were excluded. OBSERVATION PROCEDURE: Fasting plasma ghrelin, leptin, and insulin levels were assessed between 8 am and 10 am. Subjects were fed a standard breakfast, and postprandial ghrelin levels were measured 30 minutes later. RESULTS: Fasting plasma ghrelin levels negatively correlated with body mass index in both IIH subjects (r = -.48) and controls; leptin showed a positive correlation with body mass index in both IIH (r =.59) and controls. Levels were not significantly different between the groups. Postprandial ghrelin declined by 71 +/- 31 (95% CI) pg/ml in the IIH group and 71 +/- 35 (95% CI) pg/ml in the control group. CONCLUSION: Plasma ghrelin levels, both fasting and postprandial, do not differ between IIH patients and obese controls. Obese IIH patients should be encouraged to lose weight and referred for medical weight loss management to maximize their chances of alleviating their symptoms.

Adult↗