Lateral hypothalamic function in sodium chloride appetite regulation.
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CONTEXT: Increased physical activity is an integral part of weight loss programs in adolescents. We hypothesized that exercise could affect appetite-regulating hormones and the subjective desire to eat, which could partly explain the poor success rate of the existing interventions. OBJECTIVE: The objective of this study was to investigate prospectively the effects of exercise on acylated ghrelin (AG) and desacyl ghrelin (DG) concentrations and on appetite. SETTING: The setting for this study was a tertiary care center. PARTICIPANTS: Normal-weight [NW; body mass index (mean +/- se), 20.7 +/- 0.5 kg/m2] and overweight (OW; body mass index, 32.4 +/- 1.7) male adolescents (n = 17/group, age 15.3 +/- 0.2 yr) were studied. INTERVENTION: Those studied participated in 5 consecutive days of aerobic exercise (1 h/d). MAIN OUTCOME: Changes in AG and DG concentrations and in appetite during a test meal were studied. RESULTS: Exercise did not significantly affect insulin sensitivity or body weight. Fasting total (AG and DG) ghrelin concentrations were lower in OW (600 +/- 33 pg/ml) compared with NW (764 +/- 33 pg/ml, P < 0.05) boys and were not affected by exercise. In contrast, there was a differential effect of exercise on both AG and DG (P <or= 0.019). AG significantly increased after exercise, and this increase was greater in NW compared with OW adolescents (P < 0.05). Higher AG concentrations were correlated with an increase in markers of appetite (P < 0.05). CONCLUSION: Exercise differentially affects AG and DG in NW and OW male adolescents. Our data suggest that total ghrelin does not adequately reflect AG and DG concentrations and that the influence of exercise-induced hormonal changes should be considered to ensure success in weight management.
Reduced appetite combined with increased metabolic rate and decreased lean body mass is a major consequence of disease and other stressors. Studies in rodent species suggest that an understanding of appetite regulation may provide methodologies for intervention to prevent the deterioration of body mass such as observed with cancer or infectious diseases. For example, melanocortin-4 receptor (MC4-R) antagonists have shown a remarkable ability to reverse or prevent cachexia in rodents with sarcoma or treated with endotoxin. Studies in sheep have indicated that a number of peptide neurotransmitters may have a role in regulating appetite in this species. For example, agouti related protein mRNA and protein levels are dramatically altered with fasting in sheep. Moreover, agouti related protein, neuropeptide Y, melanin concentrating hormone and orexin are potent stimuli to increase feed intake in sheep. Recent studies have indicated that one of these neurotransmitters, NPY, can work in principal to improve appetite in endotoxin-treated sheep. Current studies are examining the role that MC4-R antagonists may have in the prevention or correction of body mass wasting diseases as well as practical applications in animal production.
A potential role for prolactin-releasing peptide (PrRP) in appetite regulation and hydromineral balance in goldfish was examined. PrRP was found to be expressed in discrete regions of the goldfish brain, in particular, the hypothalamus. Intraperitoneal (IP) or intracerebroventricular administration of PrRP had dose-dependent effects to suppress food intake in goldfish. Hypothalamic PrRP mRNA expression significantly increased after feeding, as well as after 7 days of food deprivation. Refeeding fish after 7 days food deprivation did not result in a postprandial increase in PrRP mRNA expression. These data suggest an anorexigenic role for PrRP in the short term around a scheduled meal time, but not over the longer term. IP injection of PrRP significantly increased pituitary prolactin (PRL) mRNA levels, suggesting involvement in the regulation of lactotroph activity. Acclimating goldfish to an ion-poor environment decreased serum osmolality and increased PrRP and PRL mRNA levels, providing evidence for PrRP involvement in hydromineral balance through its actions on lactotrophs. Acclimation to ion-poor water diminished the anorexigenic properties of PrRP in goldfish, indicating that a role for PrRP in goldfish satiation is counterbalanced by alternate systemic needs (i.e., osmoregulatory). This was further supported by an ability to reinstate the anorexigenic actions of PrRP in fish acclimated to ion-poor water by feeding a salt-rich diet. These studies provide evidence that PrRP is involved in regulating appetite and hydromineral balance in fish, and that the degree of involvement in either process varies according to overall systemic needs in response to environmental conditions.
In order to fully understand the physiological functions of adipose tissue, especially its secretory functions, and to provide a basis for the identification of novel obesity related genes, the gene expression profiling of human visceral adipose tissue was established by using cDNA array. 33P-labelled cDNA, derived from visceral adipose tissue total RNA, was hybridized to a cDNA array containing over 16,000 expressed sequence-tagged clones which represent human singleton genes. The expressed sequence tag (EST) was considered to be expressed in visceral adipose tissue when the ratio of signal to noise was greater than or equal to 2. The results were analyzed with bioinformatics. Totally, 8230 genes were found to be expressed in visceral adipose tissue with 5200 known genes and 3030 known ESTs. Most of 84 secretory proteins, 120 receptors, and 74 transcription factors expressed in adipose tissue were newly identified. Many appetite-regulating related peptides or receptors and some reproduction-related genes were first found to be expressed in adipose tissue. Eight autocrine/paracrine systems were described for the first time in the visceral adipose tissue. These results clearly demonstrate that the visceral adipose tissue has important secretory functions and there is a complex local autocrine/paracrine regulatory network. The present work suggests that the visceral adipose tissue is an important component of the neuroendocrine-immune network and plays an important role in regulating appetite not only via endocrine but also via autocrine/paracrine systems. The visceral adipose tissue might also play a role in regulating reproduction and sexual function.
BACKGROUND: Stevia is a plant-based non-nutritive sweetener. Acute effects of stevia ingestion on glycemia and hormonal responses have not been fully investigated. OBJECTIVE: This objective of this study was to evaluate the acute effects of beverages containing stevia alone and in combination with glucose on glycemic, hormonal, and appetite responses. METHODS: This study evaluated three cohorts of n=23 individuals with either normal weight (NW), overweight (OW), or type 2 diabetes mellitus (T2DM) for which each individual completed four test conditions in a randomized sequence crossover study design. The four test conditions were beverages containing stevia (75.6 mg steviol equivalents), water, glucose (30 g), and stevia+glucose (30 g glucose+75.6 mg steviol equivalents). Blood samples were collected before and for 180 min after beverage consumption. Assessments included net area under the curve (niAUC) and incremental maximal concentration values for plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1, glucagon, and PYY. Appetite was assessed with visual-analog scale questions and energy consumption during an ad libitum meal. RESULTS: Responses to the stevia beverage did not differ significantly from those for water alone, and stevia + glucose did not differ significantly from glucose alone for any of the three groups. CONCLUSION: Acute stevia consumption did not materially alter responses for glycemia or hormones involved in glucose and appetite regulation, appetite ratings, or energy intake at a subsequent meal. Clinical Trial Registry number and website where it was obtained: Clinical Trials.gov Identifier: NCT05287906. Study Details | NCT05287906 | A Trial to Assess Steviol Glycosides on Acute Appetite Hormone Release | ClinicalTrials.gov.
Anorexia, nausea and vomiting in patients with severe renal failure may cause or contribute to development of protein-energy malnutrition, which is associated with increased morbidity and mortality. However, the specific mechanisms that cause appetite suppression in uremia are poorly understood. This review summarizes the general mechanisms by which appetite is regulated. Various factors are discussed that may potentially be involved in appetite suppression in chronic renal failure.
There is substantial evidence for the role of endogenous opioid peptides in the regulation of appetite. This communication examines the possible opioid peptide mechanism(s) which are involved in appetite regulation. In the rat, activation of both the dynorphin-kappa opioid receptor and the beta-endorphin-epsilon opioid receptor appear to enhance feeding, most probably acting in different areas of the central nervous system. It also appears that rats may have a mu anorectic system. Too few studies have been undertaken to define whether the delta or sigma receptor systems are also involved in feeding responses. It is becoming apparent that a great deal of species diversity exists in the feeding responses to opiates, making it difficult to extrapolate the results obtained in rats to other species. In humans, studies with naloxone suggest an opioid sensitive feeding system which possibly is specifically involved in the regulation of carbohydrate uptake. In addition, we report here preliminary data suggesting the presence of a mu anorectic system in humans. Thus, analogous to the findings for the role of opioid receptors in analgesia, it appears that multiple opioid receptors may be involved in appetite regulation, each receptor relating to a different aspect of feeding.
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Short-term variations in caloric intake and energy expenditure-including attempts by obese patients to lose weight-tend to be modified by the body's long-term weight regulatory system. Hormones such as leptin and insulin participate in this system, which links changes in body fat content to appropriate compensatory responses in the hypothalamus. Correction of defects in the system might permit sustained weight loss in obese patients.
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Six patients with anorexia nervosa, the same patients after weight normalization, and six healthy control subjects had similar fasting and postprandial plasma cholecystokinin concentrations. These data do not support the hypothesis that low levels of hunger and food intake in anorexic patients reflect hypersecretion of this endogenous hormone, which is thought to inhibit hunger, promote satiety, and reduce feeding.
Cachexia is rarely observed in patients with advanced prostate cancer treated with combined androgen blockade. Androgens play an important role in the regulation of body mass composition and influence the secretion of leptin, the appetite regulating hormone. The aim of the study was to assess the influence of a combined treatment with nonsteroidal antiandrogen and LH-RH analogue on the hormonal regulation of appetite and changes in body mass in patients with advanced prostate cancer (Whitmore-Jewett stage D1 or D2). Eighteen patients with prostate cancer and 17 healthy subjects matched for age and body mass index were included. In all patients serum concentrations of leptin, neuropeptide Y (NPY), insulin, testosterone and estradiol were measured before and after four and twelve weeks of androgen blockade. Pretreatment serum leptin levels were similar in patients with prostate cancer and in the controls. In a multiple regression analysis only body mass index and testosterone significantly contributed to the variation of plasma leptin. During the treatment body mass and plasma leptin significantly increased while NPY decreased. The change of plasma NPY was significant only after 4 weeks of therapy. This study shows that the afferent regulation of leptin secretion is unchanged in advanced prostate cancer. Androgen ablation significantly increases body mass and influences secretion of appetite regulating hormones. Testosterone appears to play a significant role in the regulation of leptin secretion.