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PubMed2002

Functional characterizations of cocaine- and amphetamine-regulated transcript mRNA expression in rat hypothalamus.

Anatomical relationships of hypothalamic cocaine- and amphetamine-regulated transcript (CART) with other hypothalamic neuropeptides were examined by using in situ hybridization histochemistry and immunohistochemistry. CART mRNA was found in various regions in rat hypothalamus, including the periventricular nucleus, paraventricular nucleus, dorsomedial nucleus, perifornical regions, lateral nucleus, and the arcuate nucleus. In the paraventricular nucleus, CART mRNA is colocalized with vasopressin and corticotropin-releasing factor-containing neurons. Moreover, either fasting or diabetes attenuates CART mRNA expression in the hypothalamus, demonstrating that CART mRNA regulation is related to the fuel availability and peripheral hormonal status. Our findings suggest that the presence of CART mRNA in specific cell groups of the hypothalamus plays a role in hypothalamic regulation of neuroendocrine functions.

Animals↗
PubMed2002

Neuronal activation and corticotropin-releasing hormone expression in the brain of obese (fa/fa) and lean (fa/?) Zucker rats in response to refeeding.

The present study was conducted to investigate the pattern of neuronal activation and corticotropin-releasing hormone (CRH) expression in fed, food deprived and refed lean (Fa/?) and obese (fa/fa) Zucker rats. The pattern of neuronal activation was studied by measuring the expression of the immediate-early gene c-fos. Expression of c-fos and CRH mRNA was determined by in situ hybridization histochemistry. In both lean and obese rats, one hour of refeeding led to a transient increase in c-fos mRNA levels which was detected in the paraventricular hypothalamic nucleus (PVH), the dorsomedial hypothalamic nucleus, the supraoptic nucleus, the paraventricular thalamic nucleus, the central nucleus of amygdala (CeA), the lateral and medial parabrachial nuclei, the nucleus of the solitary tract, and the area postrema. In addition, refeeding led to strong activation of the arginine-vasopressin neurons located in the magnocellular part of the PVH. Following 24 h of food deprivation, CRH expression in the parvocellular division of the PVH was significantly higher in obese rats compared to lean animals. During refeeding, PVH CRH mRNA levels in obese rats decreased to reach control values. The decrease in CRH expression in obese rats was accompanied by the alleviation of the hypercorticosteronemia that characterized obese Zucker rats. CRH mRNA levels in the central nucleus of the amygdala were significantly higher in lean rats than in obese animals, when the rats were fed ad libitum During food deprivation, CeA CRH mRNA levels decreased in lean rats and gradually returned to predeprivation values during refeeding. In refed obese rats, CeA levels of CRH mRNA were higher than those of ad libitum fed or food-deprived obese mutants. In the perifornical region of the lateral hypothalamic area (LHA), the expression of CRH mRNA rose significantly in response to refeeding in lean rats, but not in obese animals. Following the first hour of refeeding, the number of neurons expressing CRH mRNA in the LHA in lean rats almost doubled. The present results demonstrate that refeeding has a stimulating effect in obese Zucker rats in a pattern of activation similar to that seen in lean Fa/? rats. They also demonstrate differences in CRH expression between Fa/? and fa/fa rats after refeeding. The most apparent of these differences was seen in the lateral hypothalamus in which refeeding failed to up-regulate CRH expression in obese rats.

Animals↗
PubMed1997

Effects of small intestinal nutrient infusion on appetite and pyloric motility are modified by age.

The mechanisms responsible for the reduction in appetite and slowing of gastric emptying in older persons are unknown. The aims of this study were to evaluate the effects of aging on small intestinal regulation of appetite and pyloric motility. Eight healthy older (age 65-75 yr) and seven healthy young (age 20-34 yr) male subjects received isocaloric (2.9 kcal/min) intraduodenal infusions of lipid and glucose for 120 min, each on separate days. During the intraduodenal infusions, perceptions of hunger, desire to eat, and fullness were assessed by visual analog scales. Pyloric motility (isolated pyloric pressure waves and tonic pyloric pressure) was measured by manometry during the intraduodenal lipid infusion. On each day, after completion of the intraduodenal nutrient infusion the subject was offered a buffet meal and food intake was quantified. Before intraduodenal nutrient infusions, sensations of hunger (P < 0.01) and desire to eat (P < 0.05) were less in the older compared with the young subjects. In the young, intraduodenal lipid suppressed hunger to a greater extent than intraduodenal glucose (P < 0.05). In older persons, neither intraduodenal nutrient infusion suppressed hunger. Intraduodenal lipid and glucose increased fullness in both age groups (P < 0.05 for both), with no significant difference between the two nutrients. There was no significant difference in food intake from the buffet meal between the elderly and young subjects. Intraduodenal lipid infusion stimulated phasic pyloric pressure waves in both age groups (P < 0.01 for both), and this response was greater (P < 0.05) in older persons. There was an increase (P < 0.01) in tonic pyloric pressure during intraduodenal lipid infusion that was not significantly different between the two age groups. We conclude that the effect of small intestinal lipid infusion on hunger is attenuated, and the stimulation of phasic pyloric pressure waves increased in healthy older persons compared with healthy young males. Increased feedback from small intestinal nutrients does not appear to be responsible for the physiological anorexia of aging.

Adult↗
PubMed2001

Feeding suppression by fibroblast growth factor-1 is accompanied by selective induction of heat shock protein 27 in hypothalamic astrocytes.

It has been suggested that fibroblast growth factor (FGF)-1 serves as a physiological satiety factor in the hypothalamus, although the molecular mechanism underlying such a function is poorly understood. To gain additional insight into this issue, we used a Sendai virus (SeV) gene expression system in rats to explore genes differentially expressed subsequent to expression of FGF-1. Using cDNA arrays, we determined that infusion of FGF-1/SeV into one lateral ventricle induced selective expression of heat shock protein (HSP) 27 in the hypothalamus. Whereas FGF-1 expression was restricted to the ependymal cell layer of the cerebral ventricles, HSP27 was more widely expressed in astrocytes residing in the surrounding periventricular region. Similarly, infusion of FGF-1 polypeptide into a lateral ventricle induced dose-dependent HSP27 expression in periventricular astrocytes surrounding the third ventricle, with maximum mRNA levels being attained 6 h after infusion. This induction of HSP27 was accompanied by a significant suppression of feeding behaviour. Interestingly, suppression of feeding caused by intracerebro ventricular infusion of ciliary neurotrophic factor was also accompanied by induction of HSP27 in periventricular astrocytes, but suppression of feeding caused by infusion of leptin was not. It therefore appears that suppression of feeding by FGF-1 is accompanied by selective induction of HSP27 expression in hypothalamic astrocytes surrounding the third ventricle, and that this response may be a key component of the mechanism by which appetite is regulated by FGF-1.

Animals↗
PubMed2001

Effect of small intestinal nutrient infusion on appetite, gastrointestinal hormone release, and gastric myoelectrical activity in young and older men.

OBJECTIVE: The mechanisms responsible for the reduction in appetite and slowing of gastric emptying in older persons are poorly understood. The aim of this study was to evaluate the effects of aging on small intestinal regulation of appetite, GI hormone release, and gastric myoelectrical activity. METHODS: Thirteen older (65-84 yr) and 13 young (18-32 yr) healthy men received isovolumetric, intraduodenal (i.d.) infusions of saline (control), lipid, and glucose for 120 min, on separate days. The energy content of the lipid and glucose infusions was identical at 2.86 kcal/min. Immediately after the i.d. infusions, each subject was offered a buffet meal, and ad libitum food intake was quantified. Blood glucose and plasma insulin, glucagon-like peptide 1, and glucose-dependent insulinotropic peptide were measured. Gastric myoelectrical activity was measured by surface electrogastrography (EGG). RESULTS: I.d. lipid suppressed food intake in both the young and older men (p < 0.05), whereas i.d. glucose suppressed food intake only in the older men (p < 0.05). The blood glucose (p < 0.01) and insulin (p < 0.05) responses to i.d. glucose were greater in older than young men. However, there were no differences in glucagon-like peptide 1 or glucose-dependent insulinotropic peptide responses to any of the infusions. There was a greater increase in the EGG power ratio both during and after i.d. glucose infusion in the young (p < 0.05) than the older men, and an attenuation of EGG frequency by nutrient infusions in older, but not young, men. CONCLUSIONS: Our findings indicate that aging is associated with nutrient-specific changes in appetite, hormonal, and gastric myoelectrical (EGG) responses to i.d. nutrients. An enhanced satiating effect of small intestinal carbohydrates may potentially contribute to the anorexia of aging.

Adolescent↗
PubMed2001

Orexin A excites serotonergic neurons in the dorsal raphe nucleus of the rat.

Orexin A (10-300 nM) strongly excited dorsal raphe serotonergic neurons maintained in vitro. The depolarization persisted in the presence of tetrodotoxin (TTX, 0.5 microM) and was associated with an increase in input resistance. These results have relevance in the context of food intake regulation and the disease, narcolepsy.

Action Potentials↗
PubMed1983

The regulation of feeding: locusts and blowflies are not so different from mammals.

The regulation of feeding in two insect groups, the locusts and the blowflies, is reviewed. The patterning of feeding is discussed first, and then the underlying mechanisms are considered in detail. The concept of "central excitability" is the key to understanding the controls of feeding. It represents a central nervous mechanism for tuning the sensitivity of the insect to food-related stimuli. The level of central excitation is influenced positively by food and also non-food stimuli, both from within and outside the animal, and negatively by deterrent stimuli and by feedbacks from peripheral systems such as stretch receptors on the gut wall, hormones and blood composition. Sustained gustatory input is required if feeding is to continue, once initiated. The level of central excitation present as a meal begins influences ingestion rate and the amounts of negative feedback tolerated before feeding stops. The duration of intervals between meals is then a function of a number of excitatory stimuli and of feeding-induced changes which reduce the likelihood of further feeding, e.g., hormone release, changes in nutrient composition or osmotic pressure of the blood, and gut distension. Other areas reviewed include changes in the regulation of feeding during the life history and the control of drinking.

Animals↗
PubMed2000

Secretory, endocrine and autocrine/paracrine function of the adipocyte.

Obesity is a major public health problem in Western countries, and >55% of adult Americans are overweight or obese. A major contributor to the epidemic of obesity is the current environment, which is characterized by increased availability of high energy foods and decreased physical activity. Several studies also demonstrated that genetic susceptibility contributes to obesity in some populations. Obesity research has focused primarily on the role of the hypothalamus in neuroendocrine regulation of food intake. However, a growing number of studies support a potential contribution of adipose tissue, via its newly discovered secretory function, to the pathogenesis of obesity and co-morbid conditions including cardiovascular disease, diabetes and hypertension. This paper will review the role of four factors secreted by adipose tissue (leptin, agouti, angiotensin II and prostaglandins) and their functions in the regulation of energy balance and whole-body homeostasis. Several other peptide and nonpeptide substances are secreted from adipose tissue; their function and regulation have been documented extensively.

Adipocytes↗
PubMed1977

Gold thioglucose obesity syndrome.

Parenteral administration of gold thioglucose to mice produces an area or necrosis in the ventromedial portion of the hypothalamus. The lesion, like lesions produced by electrocautery of this area, causes hyperphagia and consequent obesity. The glucose moiety of gold thioglucose is essential for production of the lesion. Glucose analogues (2-deoxy-glucose, sodium thioglucose and phlorizin) prevent the gold thioglucose-induced lesion, and by themselves produce a transient hyperphagia. Insulin deficiency prevents the lesion. Either adrenalectomy or hypophysectomy counteracts the effect of insulin deficiency. Electron microscopic studies, in which general necrosis is avoided by administration of aspirin before gold thioglucose or by administration of subnecrotic doses of gold thioglucose, reveal that gold thioglucose primarily affects neural elements contiguous with capillaries in the ventromedial hypothalamus. The experimental observations indicate the presence of special glucoreceptor cells in the ventromedial hypothalamus that are involved in the regulation of food intake.

Adrenalectomy↗
PubMed2004

Food deprivation decreases responsiveness of ventromedial hypothalamic neurons to melanocortins.

The melanocortin system is involved in regulation of food intake and energy balance. Melanocyte-stimulating hormone (alpha-MSH) is an endogenous melanocortin receptor (MC-R) agonist. It acts on MC3/4 receptors to reduce appetite and to increase energy expenditure. The production of alpha-MSH is reduced during food deprivation, but MC4-R density is increased. The net effect of reduced alpha-MSH production and increased receptor level is not clear. To address this question, responses of ventromedial hypothalamic (VMH) neurons to melanotan II (MTII; a synthetic analogue of alpha-MSH) were recorded in brain slices from fed and food-deprived rats. Responses to the highest dose MTII were observed in 61% of VMH neurons from fed rats but only 33% of VMH neurons from food-deprived rats. To assess a possible mechanism by which responsiveness to melanocortins is diminished even though receptor number is augmented during fasting, we examined the effect of agouti gene-related peptide (AGRP), an endogenous MC-R antagonist that stimulates food intake. The synthesis of AGRP increases during fasting. AGRP significantly reduced VMH responsiveness to MTII. Additionally, AGRP by itself evoked neuronal responses, in contrast to synthetic MC-R antagonists. AGRP (1 nM) induced a predominant inhibitory effect on VMH neurons in food-deprived rats but not in fed rats. In the presence of AGRP, MTII induced a significant inhibition of neuronal activity in deprived rats, but not in fed rats. Inhibition of VMH neurons reduces energy expenditure and the satiety signal. These findings suggest that although food deprivation increases MC4-R density, it nevertheless reduces the effectiveness of melanocortins on VMH neurons, possibly by the involvement of AGRP.

Action Potentials↗
PubMed2001

Hepatotoxic substance(s) removed by high-flux membranes enhances the positive acute phase response.

BACKGROUND: Acute phase proteins (APPs) are enhanced in end-stage renal disease patients (ESRD) requiring dialysis treatment. They are involved in a variety of pathologic processes like muscle proteolysis, cachexia, regulation of appetite, and atherosclerosis. They are predictive for mortality. APPs are not only makers but also active substances. They are mainly produced in liver cells and are primarily, but not exclusively, regulated by proinflammatory cytokines. To what extent hepatic APPs are influenced by uremic toxins is still unclear. Therefore, we investigated the effects of different ultrafiltrates (UFs) on the synthesis of alpha1-acid glycoprotein (AGP) in HepG2 cells. METHODS: A cross-sectional as well as a crossover study with high-/low-flux membranes was conducted to investigate the impact of UFs on bioactivity of liver cell cultures. Metabolic activity (MTT test), cytotoxicity (lactate dehydrogenase release), and the positive APP AGP were measured in HepG2 cells. RESULTS: Cultured hepatocytes treated with UFs from high-flux membranes exhibited a higher cytotoxicity (18.6 +/- 0.3% high-flux vs. 13.9 +/- 0.2% low-flux, P < 0.001) and a lower metabolic activity (29.3% high-flux vs. 50.3% low-flux, P < 0.001) in comparison with low-flux UFs. In addition, enhanced APP secretion could be observed under costimulatory conditions (high-flux 5.0 +/- 0.7 vs. low-flux 3.1 +/- 0.6 ng/microg protein, P < 0.05). The effects of high- and low-flux UFs were strongly expressed at the beginning and were still significantly different after 120 minutes of hemodialysis (HD) treatment. The crossover experiments confirmed that UFs collected during high-flux HD had a higher capacity to stimulate AGP synthesis in liver cells. CONCLUSION: The effects of UFs from dialysis patients demonstrate that hepatotoxic substances can be removed by dialysis. Stimulating the acute phase response UF collected during high-flux HD had a higher impact on liver cells in comparison with low-flux UF. These substances are putative cofactors involved in cytokine regulation.

Acute-Phase Reaction↗
PubMed1993

Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality.

Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selective inactivation of brain cells containing OT-receptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na(+)- and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appetite but does not appear to be essential for Na(+)-related inhibition of this important homeostatic behavior.

Animals↗
PubMed2002

Thyroid status regulates CART but not AgRP mRNA levels in the rat hypothalamus.

We examined the effects of thyroid status on cocaine- and amphetamine-regulated transcript and agouti-related peptide expression in the rat hypothalamus. Hypo- and hyperthyroidism were induced in adult male rats, and the mRNA content of cocaine- and amphetamine-regulated transcript and agouti-related peptide was determined using in situ hybridization. Hyperthyroidism induces a reduction in cocaine- and amphetamine-regulated transcript mRNA levels in the paraventricular nucleus, without any change in the arcuate and dorsomedial nuclei and in the lateral hypothalamic area. On the other hand, hypothyroidism had not effect on cocaine- and amphetamine-regulated transcript expression in any of these nuclei. Agouti-related peptide expression in the arcuate nucleus was not affected by the thyroid status. These data indicate that the increments in food intake in hyperthyroidism could be mediated, at least in some extent, by a decreased expression, at the paraventricular nucleus of the hypothalamus, of the anorexigenic cocaine- and amphetamine-regulated transcript peptides.

Agouti-Related Protein↗