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At least 613 records · Page 34Linked to original sources
PubMed2004

Roles of corticotropin-releasing factor, neuropeptide Y and corticosterone in the regulation of food intake in Xenopus laevis.

In mammals, hypothalamic control of food intake involves counterregulation of appetite by an orexigenic peptides such as corticotropin-releasing factor (CRF), and orexigenic peptides such as neuropeptide Y (NPY). Glucocorticoids also stimulate food intake by inhibiting CRF while facilitating NPY actions. To gain a better understanding of the diversity and evolution of neuroendocrine feeding controls in vertebrates, we analysed the effects of CRF, NPY and glucocorticoids on food intake in juvenile Xenopus laevis. We also analysed brain CRF and NPY mRNA content and plasma corticosterone concentrations in relation to nutritional state. Intracerebroventricular (i.c.v.) injection of ovine CRF suppressed food intake while CRF receptor antagonist alpha helical CRF(9-41) significantly increased food intake relative to uninjected and placebo controls. By contrast, i.c.v. injection of frog NPY and short-term corticosterone treatment increased food intake. Semi-quantitative reverse transcription-polymerase chain reaction analyses showed that CRF and NPY mRNA fluctuated with food intake in the brain region containing the mid-posterior hypothalamus, pretectum, and optic tectum: CRF mRNA decreased 6 h after a meal and remained low through 31 days of food deprivation; NPY mRNA content also decreased 6 h after a meal, but increased to prefeeding levels by 24 h. Plasma corticosterone concentration increased 6 h after a meal, returned to prefeeding levels by 24 h, and did not change with prolonged food deprivation. This postprandial increase in plasma corticosterone may be related to the subsequent increase in plasma glucose and body water content that occurs 24 h postfeeding. Overall, our data support the conclusion that, similar to other vertebrates, CRF is anorexigenic while NPY is orexigenic in X. laevis, and CRF secretion modulates food intake in the absence of stress by exerting an inhibitory tone on appetite. Furthermore, the stress axis is activated in response to food intake, but in contrast to mammals and birds is not activated during periods of food deprivation.

Adaptation, Physiological↗
PubMed1999

Heritability of hunger relationships with food intake in free-living humans.

The heritability of the before and after meal self-ratings of hunger and thirst and their relationship to food intake was investigated with 110 identical and 102 fraternal same-sex and 53 fraternal mixed-gender adult twin pairs who were paid to maintain 7-day food intake diaries. From the diary reports, the total and meal intakes of food energy and the amounts of the macronutrients ingested were estimated. Subjects rated their subjective levels of hunger on a seven-point scale both before and after eating. Linear structural modeling was applied to investigate the nature and degree of genetic and environmental influences and revealed significant genetic influences on the self-rated levels of hunger both before and after the meals and the change in hunger over the meal. In addition, the relationship between hunger and intake was influenced by the genes. Significant heritabilities were found for the correlations, and the slopes of the regression lines relating before-meal hunger to meal size and also the change in hunger over the meal to intake. This indicates that hunger's effect on intake and, in turn, intake's effects on hunger are to some extent heritable. This suggests that the level of subjective experience and the individuals responses to them are influenced by the genes and become part of the total package of genetically determined physiological, socio/cultural, and psychological processes that regulate energy balance.

Adult↗
PubMed2001

Heritability of diurnal changes in food intake in free-living humans.

OBJECTIVES: The time of day of meal ingestion, the number of people present at the meal, the subjective state of hunger, and the estimated before-meal contents in the stomach have been established as influences on the amount eaten in a meal, and this influence has been shown to be heritable. Because these factors intercorrelate, the possibility that the calculated heritabilities for some of these variables could result indirectly from their convariation with one of the other heritable variables was assessed. METHODS: The independence of the heritability of the influence of these four factors was investigated with 110 identical and 102 fraternal same-sex and 53 fraternal mixed-sex adult twin pairs who were paid to maintain 7-d food intake diaries. From the diary reports, the meal sizes were calculated and subjected to multiple regression analysis using the estimated before-meal stomach contents, the reported number of other people present, the subjective hunger ratings, and the time of day of the meal as predictors. Linear structural modeling was applied to the beta coefficients from the multiple regression to investigate whether the heritability of the influences of these four variables was independent. RESULTS: Significant genetic effects were found for the beta coefficients for all four variables, indicating that the heritability of their relationship with intake is to some extent heritable. CONCLUSIONS: These results suggest that the influences of multiple factors on intake are influenced by the genes and become part of the total package of genetically determined physiologic, sociocultural, and psychological processes that regulate energy balance.

Adult↗
PubMed2002

Independence of heritable influences on the food intake of free-living humans.

OBJECTIVE: The time of day of meal ingestion, the number of people present at the meal, the subjective state of hunger, and the estimated before-meal contents in the stomach have been established as influences on the amount eaten in a meal and these influences have been shown to be heritable. Because these factors intercorrelate, the calculated heritabilities for some of these variables might result indirectly from their covariation with one of the other heritable variables. The independence of the heritability of the influence of these four factors was investigated with 110 identical and 102 fraternal same-sex and 53 fraternal mixed-sex adult twin pairs who were paid to maintain 7-d food-intake diaries. METHODS: From the diary reports, the meal sizes were calculated and subjected to multiple regression analysis using the estimated before-meal stomach contents, the reported number of other people present, the subjective hunger ratings, and the time of day of the meal as predictors. Linear structural modeling was applied to the beta-coefficients from the multiple regression to investigate whether the heritability of the influences of these four variables was independent. RESULTS: Significant genetic effects were found for the beta-coefficients for all four variables, indicating that the heritability of their relationship with intake is to some extent independent and heritable. CONCLUSIONS: This suggests that influences of multiple factors on intake are influenced by the genes and become part of the total package of genetically determined physiologic, sociocultural, and psychological processes that regulate energy balance.

Adult↗
PubMed2001

Control of food intake in the obese.

Food intake (eating) is a form of behavior that is subject to conscious control. In practice, many obese and weight-gaining individuals claim that their eating is out of (their) control. Mechanistic models describe the interplay of biological and environmental forces that control food intake. However, because human food intake is characterized by individuals intervening to adjust their own patterns of behavior, food intake should reflect interactions among biology, environment, and attempted self-imposed control of behavior. In general, humans display a system of weight regulation that is asymmetrical--a reduction in body weight is strongly defended but weight gain is not. The body seems to tolerate a positive energy balance. There is no mechanism that can detect a positive energy balance per se or that can implement a sufficiently strong correction to behavior to maintain body weight in an environment that promotes consumption. The evolutionary process has favored biological traits associated with preferences for high energy density (sweet and/or fatty) energy-yielding foods. The control of food intake in obese or weight-gaining individuals may display various risk factors that favor an increase in energy. These include the preference for high energy-dense over low energy-dense foods, weak postprandial inhibitory signaling, strong hunger traits associated with low leptin levels after weight loss, and the consumption of fatty foods. In addition, many individuals (up to 47% of some samples) display binge eating patterns, whereas approximately 16% show either night eating or nocturnal eating. Because energy expenditure is only loosely coupled to energy intake, sedentariness does not down-regulate food intake.

Appetite Regulation↗
PubMed2005

Role of thyroid hormone deiodination in the hypothalamus.

Iodothyronine deiodinases (D1, D2, and D3) comprise a family of selenoproteins that are involved in the conversion of thyroxine (T(4)) to active triiodothyronine (T(3)), and also the inactivation of both thyroid hormones. The deiodinase enzymes are of critical importance for the normal development and function of the central nervous system. D1 is absent from the human brain, suggesting that D2 and D3 are the two main enzymes involved in the maintenance of thyroid hormone homeostasis in the central nervous system, D2 as the primary T(3)-producing enzyme, and D3 as the primary inactivating enzyme. While the coordinated action of D2 and D3 maintain constant T(3) levels in the cortex independently from the circulating thyroid hormone levels, the role of deiodinases in the hypothalamus may be more complex, as suggested by the regulation of D2 activity in the hypothalamus by infection, fasting and changes in photoperiod. Tanycytes, the primary source of D2 activity in the hypothalamus, integrate hormonal and probably neuronal signals, and under specific conditions, may influence neuroendocrine functions by altering local T(3) tissue concentrations. This function may be of particular importance in the regulation of the hypothalamic-pituitary-thyroid axis during fasting and infection, and in the regulation of appetite and reproductive function. Transient expression of D3 in the preoptic region during a critical time of development suggests a special role for this deiodinase in sexual differentiation of the brain.

Animals↗
PubMed2003

Hyperthyroidism is associated with suppressed circulating ghrelin levels.

Ghrelin stimulates GH secretion as well as appetite and food intake. To explore whether ghrelin is involved in the regulation of appetite and body weight in hyperthyroidism, circulating ghrelin levels were measured in nine hyperthyroid patients before and after medical treatment and compared with those in eight healthy control subjects. All participants were studied in the postabsorptive state and during a 3-h euglycemic hyperinsulinemic clamp. Before treatment the patients had 3- to 5-fold elevations of T(3), and during treatment the patients gained 5 kg of body weight. Ghrelin levels were decreased in hyperthyroidism both in the fasting state (hyperthyroid, 1080 +/- 195 pg/ml; euthyroid, 1480 +/- 215 pg/ml; P = 0.03) and during clamp (hyperthyroid, 833 +/- 150 pg/ml; euthyroid, 1210 +/- 180 pg/m; P = 0.02). After treatment, ghrelin levels did not differ from those in control subjects. In all three study groups the clamp significantly reduced ghrelin levels compared with fasting levels. In conclusion, ghrelin levels are reduced in hyperthyroidism and become normalized by medical antithyroid treatment. Hyperinsulinemia suppresses ghrelin regardless of thyroid status. Ghrelin is not a primary stimulator of appetite and food intake in hyperthyroidism, and the mechanisms underlying the suppressive effect of hyperthyroidism on ghrelin secretion remain unclear.

Adult↗
PubMed1998

Ectopic expression of the CRF-binding protein: minor impact on HPA axis regulation but induction of sexually dimorphic weight gain.

Corticotrophin-releasing factor (CRF) and urocortin possess a high-affinity binding protein. Although the CRF binding protein (BP) can sequester these ligands and inhibit their activity, the endogenous activity of this protein is not understood. Therefore, transgenic mouse lines that over-express the CRF-BP were created. The transgene was constructed by ligating rat CRF-BP cDNA (1.1 kb) between a mouse metallothionein-I promoter (1.8 kb) and a nonfunctional human growth hormone gene sequence (2.1 kb) in a modified pBR322 plasmid and microinjecting the transgene into C57BL/6 x SJL hybrid ova. The transgene was expressed in 50% in both male and female progeny. All transgenic lines were maintained by crossing transgenic animals with wild-type C57BL/6 mates. Reverse-transcriptase (RT) PCR of the CRF-BP transgene showed that it is widely expressed not only in the brain and pituitary, but also peripheral tissues including the liver, kidney and spleen. Transgenic animals of both sexes showed significant increases in weight gain as established by analysis of variance; however, the weight gain profiles for each sex were distinct. High levels of circulating CRF-BP were detected in the transgenic animals, but the basal ACTH and corticosterone levels were not significantly decreased compared to wild-type littermates. The hypothalamopituitary-adrenal (HPA) axis was stimulated by systemic inflammation induced with lipopolysaccharide (LPS). An expected increase in transgene expression was observed and was accompanied by a significant attenuation of ACTH secretion at 3 h after LPS injection in the transgenic males but not the females. These data suggest that HPA axis regulation is significantly affected only with very high circulating levels of CRF-BP. Moreover, this work supports previous studies that implicate CRF and urocortin in the regulation of appetite and the binding protein expression may play a sexually dimorphic role in regulating this and other responses.

Adrenal Glands↗
PubMed2003

Cardiovascular effects of leptin and orexins.

Leptin, the product of the ob gene, is a satiety factor secreted mainly in adipose tissue and is part of a signaling mechanism regulating the content of body fat. It acts on leptin receptors, most of which are located in the hypothalamus, a region of the brain known to control body homeostasis. The fastest and strongest hypothalamic response to leptin in ob/ob mice occurs in the paraventricular nucleus, which is involved in neuroendocrine and autonomic functions. On the other hand, orexins (orexin-A and -B) or hypocretins (hypocretin-1 and -2) were recently discovered in the hypothalamus, in which a number of neuropeptides are known to stimulate or suppress food intake. These substances are considered important for the regulation of appetite and energy homeostasis. Orexins were initially thought to function in the hypothalamic regulation of feeding behavior, but orexin-containing fibers and their receptors are also distributed in parts of the brain closely associated with the regulation of cardiovascular and autonomic functions. Functional studies have shown that these peptides are involved in cardiovascular and sympathetic regulation. The objective of this article is to summarize evidence on the effects of leptin and orexins on cardiovascular function in vivo and in vitro and to discuss the pathophysiological relevance of these peptides and possible interactions.

Animals↗