Circadian Rhythm Of Food Intake Research Articles

Dietary protein load affects the energy and nitrogen balance requiring liver glutamate dehydrogenase to maintain physical activity

Provision of amino acids to the liver is instrumental for gluconeogenesis while it requires safe disposal of the amino group. The mitochondrial enzyme glutamate dehydrogenase (GDH) is central for hepatic ammonia detoxification by deaminating excessive amino acids towards ureagenesis and preventing hyperammonemia. The present study investigated the early adaptive responses to changes in dietary protein intake in control mice and liver-specific GDH knockout mice (Hep-Glud1-/-). Mice were fed chow diets with a wide coverage of protein contents; i.e. suboptimal 10%, standard 20%, over optimal 30%, and high 45% protein diets; switched every 4 days. Metabolic adaptations of the mice were assessed in calorimetric chambers before tissue collection and analyses. Hep-Glud1-/- mice exhibited impaired alanine induced gluconeogenesis and constitutive hyperammonemia. The expression and activity of GDH in liver lysates were not significantly changed by the different diets. However, applying an in situ redox-sensitive assay on cryopreserved tissue sections revealed higher hepatic GDH activity in mice fed the high-protein diets. On the same section series, immunohistochemistry provided corresponding mapping of the GDH expression. Cosinor analysis from calorimetric chambers showed that the circadian rhythm of food intake and energy expenditure was altered in Hep-Glud1-/- mice. In control mice, energy expenditure shifted from carbohydrate to amino acid oxidation when diet was switched to high protein content. This shift was impaired in Hep-Glud1-/- mice and consequently the spontaneous physical activity was markedly reduced in GDH knockout mice. These data highlight the central role of liver GDH in the energy balance adaptation to dietary proteins.

PS-B07-11: EFFECT OF TRF INTERVENTION ON DIET INDUCED OBESITY: A NON-PHARMACOLOGICAL THERAPEUTIC STRATEGY

Objectives: Time-restricted feeding (TRF) regulates the circadian rhythm of food intake that protects against metabolic disorders. The aim of our study are 12 hours time restricted feeding effects on diet induces obesity in rats model. Material & Method: Total 21 Wistar rats were included i.e. control, TRF and High Fat diet (HFD) group. HFD group was fed with fatty diet at ad lib for two months and shifted to TRF (12 hours feeding i.e 8:00pm - 8:00am) for three months, after which they were again put back on ad lib. TRF group fed chow diet during 8:00pm to 8:00am for three months and then these rats shifted to ad lib for three months. Control group fed chow diet at ad lib. Body weight was calculated and blood samples were collected to measure blood glucose, insulin, lipid profile and gene expression. Results: The body weight of HFD group were significantly increased and TRF with chow diet were significantly decreased as compared to control rats (p = 0.0263) and (p = 0.0054) respectively. The level of HDL was reduced in rats fed with HFD whereas total cholesterol, TG and LDL were increased. TRF intervention with HFD diet reduced body weight, blood glucose level, TG and LDL and elevated the level of insulin, total cholesterol and HDL. Per1 and Bmal1 gene were up regulated in HFD group and after TRF intervention had reduced mRNA expression. TRF intervention with HFD and chow diet showed its legacy effect when put on ad lib. Conclusion: TRF intervention is easily adaptable lifestyle modification and non-pharmacological strategy can reduces the risk factor of obesity and its associated metabolic disorders.

Time-restricted eating as a novel strategy for treatment of obesity and it's comorbid conditions

The article provides a review of the current literature about time-restricted eating (TRE) as a new tool for the treatment of obesity and comorbid conditions. The search for new nutritional strategies in obesity, one of which is TRE, is due to the weak adherence of patients to hypocaloric diets in the long term, as well as the available data on the importance of -desynchronization of food intake with natural circadian rhythms in the development and progression of obesity and cardio--metabolic complications. The article describes the main mechanisms that regulate the circadian rhythms of food intake and nutrient absorption, substantiates the importance of adhering to a physiological diet for maintaining metabolic health. The main part of the review is devoted to reviewing the currently available researches on the effectiveness of various strategies of intermittent energy restriction for weight loss and the correction of metabolic parameters. Potential mechanisms of the -effect of TRE on health are discussed, including those mediated by an unintentional decrease in caloric intake and changes in eating behavior, and differences in the effectiveness of early and late TRE. The article contains a detailed discussion of the potential problems and contradictions associated with the use of time-restricted eating in clinical practice, namely: the limitations and inconsistencies of the available clinical trials, the lack of data on long-term efficacy and safety, social and psychological limitations that impede the widespread use of TRE.

Adaptation of the night eating questionnaire for Brazilian adolescents.

IntroductionNight Eating Syndrome (NES) is characterized by a delay in the circadian rhythm of food intake and affects 1.5% of the general population, occurring more frequently in obese people. The Night Eating Questionnaire (NEQ) was originally developed for the American adult population. It is a self-administered instrument widely used in the identification and follow-up of individuals with NES. Although the NEQ has been translated and validated for Brazilian adults, there are no reports of its adaptation for use in Brazilian adolescents. The present study aimed to adapt and evaluate reliability and reproducibility of the NEQ for Brazilian adolescents.Material and MethodsInitially, a semantic adaptation of the Portuguese version of the NEQ was performed by 3 professionals with experience with adolescents. The suggested text was analyzed and consolidated item by item by the researchers and then presented to 21 adolescents from an intermediate school in Fortaleza. The questions with low level of understanding (<90%) were modified and the questionnaire was re-applied to 23 adolescents, obtaining satisfactory understanding.ResultsThe version of the NEQ for Brazilian adolescents, compared to the adult version, contains changes in items 3, 5, 6, 7 and 13. The questionnaire was administered to 463 students aged 11 to 17 years (mean ± SD = 13.7 ± 1.2), from 3 schools. The internal consistency, measured by the Cronbach's alpha coefficient, was 0.73. The reproducibility that was measured after one week in 27 adolescents was 0.92 (95% CI 0.82-0.96).ConclusionThe new version of the NEQ for Brazilian adolescents presents excellent reproducibility and good internal consistency and is a simple and useful instrument to evaluate nocturnal eating symptoms in this age group.

Liver Glutamate Dehydrogenase Controls Whole-Body Energy Partitioning Through Amino Acid-Derived Gluconeogenesis and Ammonia Homeostasis.

Ammonia detoxification and gluconeogenesis are major hepatic functions mutually connected through amino acid metabolism. The liver is rich in glutamate dehydrogenase (GDH) that catalyzes the reversible oxidative deamination of glutamate to α-ketoglutarate and ammonia, thus bridging amino acid-to-glucose pathways. Here we generated inducible liver-specific GDH-knockout mice (HepGlud1-/- ) to explore the role of hepatic GDH on metabolic homeostasis. Investigation of nitrogen metabolism revealed altered ammonia homeostasis in HepGlud1-/- mice characterized by increased circulating ammonia associated with reduced detoxification process into urea. The abrogation of hepatic GDH also modified energy homeostasis. In the fasting state, HepGlud1-/- mice could barely produce glucose in response to alanine due to impaired liver gluconeogenesis. Compared with control mice, lipid consumption in HepGlud1-/- mice was favored over carbohydrates as a compensatory energy fuel. The changes in energy partitioning induced by the lack of liver GDH modified the circadian rhythm of food intake. Overall, this study demonstrates the central role of hepatic GDH as a major regulator for the maintenance of ammonia and whole-body energy homeostasis.

Expression of the clock gene Rev-erbα in the brain controls the circadian organisation of food intake and locomotor activity, but not daily variations of energy metabolism.

The nuclear receptor REV-ERBα is part of the molecular clock mechanism and is considered to be involved in a variety of biological processes within metabolically active peripheral tissues as well. To investigate whether Rev-erbα (also known as Nr1d1) in the brain plays a role in the daily variations of energy metabolism, feeding behaviour and the sleep-wake cycle, we studied mice with global (GKO) or brain (BKO) deletion of Rev-erbα. Mice were studied both in a light/dark cycle and in constant darkness, and then 24-hour variations of Respiratory quotient (RQ) and energy expenditure, as well as the temporal patterns of rest-activity and feeding behaviour, were recorded. The RQ increase of GKO mice was not detected in BKO animals, indicating a peripheral origin for this metabolic alteration. Arrhythmic patterns of locomotor activity were only found in BKO mice. By contrast, the circadian rhythm of food intake was lost both in GKO and BKO mice, mostly by increasing the number of daytime meals. These changes in the circadian pattern of feeding behaviour were, to some extent, correlated with a loss of rhythmicity of hypothalamic Hcrt (also named Orx) mRNA levels. Taken together, these findings highlight that Rev-erbα in the brain is involved in the temporal partitioning of feeding and sleep, whereas its effects on energy metabolism are mainly exerted through its peripheral expression.

Extreme obesity is associated with variation in genes related to the circadian rhythm of food intake and hypothalamic signaling.

The hypothalamus is important for regulation of energy intake. Mutations in genes involved in the function of the hypothalamus can lead to early-onset severe obesity. To look further into this, we have followed a strategy that allowed us to identify rare and common gene variants as candidates for the background of extreme obesity from a relatively small cohort. For that we focused on subjects with a well-selected phenotype and on a defined gene set and used a rich source of genetic data with stringent cut-off values. A list of 166 genes functionally related to the hypothalamus was generated. In those genes complete exome sequence data from 30 extreme obese subjects (60 genomes) were screened for novel rare indel, nonsense, and missense variants with a predicted negative impact on protein function. In addition, (moderately) common variants in those genes were analyzed for allelic association using the general population as reference (false discovery rate<0.05). Six novel rare deleterious missense variants were found in the genes for BAIAP3, NBEA, PRRC2A, RYR1, SIM1, and TRH, and a novel indel variant in LEPR. Common variants in the six genes for MBOAT4, NPC1, NPW, NUCB2, PER1, and PRRC2A showed significant allelic association with extreme obesity. Our findings underscore the complexity of the genetic background of extreme obesity involving rare and common variants of genes from defined metabolic and physiologic processes, in particular regulation of the circadian rhythm of food intake and hypothalamic signaling.

Effects of early weaning on the circadian rhythm and behavioral satiety sequence in rats

The objective of this work was to study the effect of early weaning on circadian rhythm and the behavioral satiety sequence in adult rats. Male Wistar rat pups were weaned for separation from the mother at 15 (D15), 21 (D21) and 30 (D30) days old. Body weight and food intake was measured every 30 days until pups were 150 days old. At 90 days of age, the circadian rhythm of food intake was evaluated every 4h for three days. Behavioral satiety was evaluated at 35 and 100 days of age. This work demonstrated that body weight and food intake were not altered, but the behavioral satiety sequence demonstrated that the D15 group delayed satiety compared with the D30 group at 100 days of age. In the circadian rhythm of the food intake study, early weaning (D15) changed food intake in the intermediary period of the light phase and in the intermediary period of the dark phase. In conclusion, our study showed that early weaning may alter the feeding behavior mainly in relation to satiety and the circadian rhythm of feeding. It is possible that the presence of other environmental stimuli during early weaning can cause hyperphagia and deregulate the mechanisms of homeostasis and body weight control. This study supports theories that depict insults during early life as determinants of chronic diseases.

The supply chain of the brain &ndash; An economic approach to human energy metabolism

Event Abstract Back to Event The supply chain of the brain – An economic approach to human energy metabolism Dirk Langemann1* 1 Technische Universität Braunschweig, Institute of Computational Mathematics, Germany The description of the human metabolism from the food intake to the energy consumption in the body periphery and in the brain includes a tremendous number of regulatory pathways and involved substances. The abstraction from energy supporting and transporting substances to energy contents in selected compartments and the summarization of redundant regulatory pathways leads to integrated models of the metabolism. It is the clarity of these models, which allows us to develop a systemic understanding of the human metabolism as a whole by mathematical methods, in particular by the theory of dynamical systems. The named integrated models are supply chains, which are well-discussed in economics and logistics. In analogy to the systemic investigation of the metabolism, the economical mechanisms are not completely quantified although their basic directions of regulation are without any doubt. Nevertheless, worthwhile qualitative explanations are derived. Following this approach, the metabolism is regarded as an energy supply chain from the food intake to the final energy consumers in the organism. The complex and not completely quantified regulatory mechanisms are abstracted to their pull and push components, which mathematically speaking corresponds to a linearization. The pull component of a flux is the part regulated by the receiver, the push component is the part governed by the supplier. Robust modeling techniques assure the conservation of the qualitative behavior of the dynamical systems. The simple distinction between pull and push component yields qualitative properties of the considered dynamical system. Economic supply chains as well as metabolic supply chains with dominating pull component show a retrograde propagation of perturbation. Hence, effects of perturbations are found in front of their causes with respect to the transport direction. This implies that the cause of an obese body is behind the body compartment in the supply chain. Consequently, the Selfish-brain theory assumes the cause to be located in the brain. Integrated models are used to support such assumptions, e.g. the observation of a circadian rhythm of food intake requires the existence of a relevant energy consuming compartment behind the body compartment. Thus, the brain as energy consumer becomes an indispensable compartment in a systemic metabolism model. Beside the theoretical use of a comprehensible model frame for analyzing the metabolism and its pathologies, we present selected clinical applications where the systemic understanding of the human metabolism directly indicates therapeutic interventions. Future work will deal with the inclusion of the metabolic memory, the stress axis or the sleep rhythm into the integrated model. Conference: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour, 23554 Luebeck, Germany, 27 May - 28 May, 2010. Presentation Type: Oral Presentation Topic: Talks Citation: Langemann D (2010). The supply chain of the brain – An economic approach to human energy metabolism. Front. Neurosci. Conference Abstract: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour. doi: 10.3389/conf.fnins.2010.08.00002 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 12 Apr 2010; Published Online: 12 Apr 2010. * Correspondence: Dirk Langemann, Technische Universität Braunschweig, Institute of Computational Mathematics, Braunschweig, Germany, d.langemann@tu-bs.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Dirk Langemann Google Dirk Langemann Google Scholar Dirk Langemann PubMed Dirk Langemann Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

A biobehavioural model of the night eating syndrome

This paper will propose a biobehavioral mechanism for the Night Eating Syndrome (NES), a disorder characterized by a delayed circadian rhythm of food intake and neuroendocrine function. Food intake consists of at least 25% of daily caloric intake after the evening meal and/or at least two nighttime awakenings with ingestions per week. This will be explored by reviewing neuroimaging of brain serotonin transporters (SERT) and treatment with selective serotonin reuptake inhibitors (SSRIs). SERT binding is elevated in the midbrain of night eaters, causing dysregulation of the circadian rhythm of both food intake and neuroendocrine function. The administration of SSRIs blocks the reuptake of serotonin and restores the circadian rhythm of both food intake and neuroendocrine function. This hypothesis implies that reduction of SERT activity should increase postsynaptic serotonin transmission and relieve NES. This is precisely the effect of SSRIs. NES is a function of elevated SERT, and blocking of SERT with an SSRI resolves NES. This model of NES attests to the validity of the diagnosis of NES and the criteria by which it is identified, and it provides an explanation of the mechanism.

Circadian Rhythm Profiles in Women with Night Eating Syndrome

Night eating syndrome (NES) is characterized by evening hyperphagia and frequent awakenings accompanied by food intake. Patients with NES display a delayed circadian pattern of food intake but retain a normal sleep-wake cycle. These characteristics initiated the current study, in which the phase and amplitude of behavioral and neuroendocrine circadian rhythms in patients with NES were evaluated. Fifteen women with NES (mean age +/- SD, 40.8 +/- 8.7 y) and 14 control subjects (38.6 +/- 9.5 y) were studied in the laboratory for 3 nights, with food intake measured daily. Blood also was collected for 25 h (every 2 h from 0800 to 2000 h, and then hourly from 2100 to 0900 h) and assayed for glucose and 7 hormones (insulin, ghrelin, leptin, melatonin, cortisol, thyroid-stimulating hormone [TSH] and prolactin). Statistical analyses utilized linear mixed-effects cosinor analysis. Control subjects displayed normal phases and amplitudes for all circadian rhythms. In contrast, patients with NES showed a phase delay in the timing of meals, and delayed circadian rhythms for total caloric, fat, and carbohydrate intake. In addition, phase delays of 1.0 to 2.8 h were found in 2 food-regulatory rhythms-leptin and insulin-and in the circadian melatonin rhythm (with a trend for a delay in the circadian cortisol rhythm). In contrast, circulating levels of ghrelin, the primary hormone that stimulates food intake, were phase advanced by 5.2 h. The glucose rhythm showed an inverted circadian pattern. Patients with NES also showed reduced amplitudes in the circadian rhythms of food intake, cortisol, ghrelin, and insulin, but increased TSH amplitude. Thus, patients with NES demonstrated significant changes in the timing and amplitude of various behavioral and physiological circadian markers involved in appetite and neuroendocrine regulation. As such, NES may result from dissociations between central (suprachiasmatic nucleus) timing mechanisms and putative oscillators elsewhere in the central nervous system or periphery, such as the stomach or liver. Considering these results, chronobiologic treatments for NES such as bright light therapy may be useful. Indeed, bright light therapy has shown efficacy in reducing night eating in case studies and should be evaluated in controlled clinical trials.

Modeling circadian rhythms of food intake by means of parametric deconvolution: results from studies of the night eating syndrome

BackgroundDisordered temporal eating patterns are a feature of a number of eating disorders. There is currently no standard mathematical model to quantify temporal eating patterns. ObjectiveWe aimed to develop a simple model by which to describe the temporal eating patterns of adult humans. For this purpose, patients with the night eating syndrome (NES) and persons without an eating disorder were assessed. DesignData were obtained from 2 studies, each involving patients with NES and control subjects. Data were analyzed by means of a novel equation to describe the 24-h temporal eating patterns. The equation employed the integration over time of 3 Gaussian equations to describe the cumulative daily caloric intake. ResultsThe new model accurately described and quantified the temporal eating patterns of the subjects in the 2 studies. The analyses showed differences in the temporal eating patterns and in the amount of intake of normal-weight and overweight subjects with NES. ConclusionsThis novel model can be used to accurately and objectively describe and quantify temporal food intake patterns. It can also be used to establish norms for various human populations.

Serotonergic mechanisms in the night eating syndrome.

This review describes new findings regarding the Night Eating Syndrome (NES), a distinct disorder that is precipitated by stress most persons who suffer from it. It is manifested by a delayed circadian rhythm of food intake (evening hyperphagia, nighttime awakenings with ingestions and morning anorexia) with an intact circadian sleep rhythm. It is readily diagnosed by calibrated diagnostic instruments and has been widely reported in the medical literature. NES has genetic determinants and is more prevalent than the traditional eating disorders. New findings suggest that it represents a dysregulation of serotonin function. Thus, SPECT (single-positron-emission computerized tomography) has shown greatly elevated serotonin transporter binding in the midbrain of night eaters. This appears to impair postsynaptic serotonin transmission in areas mediating circadian rhythms and food intake. Restoration of serotonergic function with SSRIs (selective serotonin reuptake inhibitors) in four clinical trials has resulted in a great decrease in night eating behaviors and significant weight loss among overweight and obese night eaters.

A Paradigm for Facilitating Pharmacotherapy at a Distance

To test a novel method of facilitating pharmacotherapy at a distance and assess the effectiveness of sertraline for the treatment of night eating syndrome (NES). The effectiveness of the selective serotonin reuptake inhibitor sertraline in the treatment of NES was assessed at a distance. NES is characterized by a delay in the circadian rhythm of food intake, with evening hyperphagia and/or nighttime awakenings and ingestions. Persons who contacted us through our Web site, e-mail, or telephone for help with their NES completed a Night Eating Questionnaire and received a semistructured interview (Night Eating Syndrome History and Inventory) to determine the presence of NES. Fifty such persons received treatment with sertraline from their own physicians, to whom we offered consultation. Participants completed questionnaires every 2 weeks for 8 weeks and received a final telephone interview to assess their progress. Outcomes were compared with those from an earlier face-to-face open-label trial of sertraline. The study was conducted from September 2003 to May 2005. Both the questionnaires and interviews showed improvements in 5 key aspects of NES: the general Night Eating Symptom Scale, evening hyperphagia, nighttime awakenings, nocturnal ingestions, and the Beck Depression Inventory (all p < .001), and the mean body weight of the 41 overweight and obese subjects, reported by survey, fell 3.0 kg (p = .01). These results are similar to those obtained in an earlier face-to-face trial of sertraline with NES. The study confirmed the effectiveness of sertraline in the treatment of NES and introduced a paradigm for facilitating pharmaco-therapy at a distance.

Attenuation of circadian rhythms of food intake and respiration in aging diabetes-prone BHE/Cdb rats.

The hypothesis that BHE/Cdb rats with mutations in their mitochondrial genome might accommodate this mutation by changing their food intake patterns was tested. Four experiments were conducted. Experiments 1 and 2 examined food intake patterns of BHE/Cdb rats fed a stock diet or BHE/Cdb and Sprague-Dawley rats fed a high-fat diet from weaning. Experiment 3 examined the daily rhythms of respiration and heat production in these rats at 200 days of age. Experiment 4 examined the effects of diet composition on these measurements at 50-day intervals. The Sprague-Dawley rats, regardless of diet, had the typical day-night rhythms of feeding and respiration. In contrast, the BHE/Cdb rats fed the high-fat diet showed normal rhythms initially, but with age, these rhythms were attenuated. The changes in rhythms preceded the development of glucose intolerance.

Chapter 18 SCN output drives the autonomic nervous system: with special reference to the autonomic function related to the regulation of glucose metabolism

Publisher Summary This chapter describes the role of the suprachiasmatic nucleus (SCN) in the control of the autonomic nervous system with respect to the mechanism of glucose homeostasis. In the effort to elucidate the mechanism of circadian rhythms of food intake and energy metabolism using rats as experimental animals, the chapter finds evidence that the hypothalamic SCN has an important role in the regulation of glucose metabolism through the control of the autonomic nerves. When SCN vasoactive intestinal polypeptide (VIP) neurons receive signals from the circadian oscillator, they may transmit signals for a circadian rhythm to the autonomic functions that include mechanism to maintain glucose homeostasis. When these VIP neurons may receive signals of changes in outer and inner environments, they may produce signals for the alterations in the autonomic nerves and ensure survival, especially in the excitement of sympathetic nervous system related to the elevation of the blood glucose under stressful conditions.

Effects of selective vagotomy on circadian rhythms of plasma glucose, insulin and food intake in control and ventromedial hypothalamic (VMH) lesioned rats.

Effects of hepatic and celiac vagotomy on circadian rhythms of plasma glucose, insulin, and food intake were examined in sham-operated (control) and ventromedial hypothalamic (VMH) lesioned rats. Rats were acclimated to the condition with a 12-hour light-dark cycle for 1 week before surgery. One week after VMH lesions, control and VMH lesioned rats were divided into three groups: sham vagotomy, hepatic vagotomy, and celiac vagotomy. Three days after vagotomy, food intake was measured at 6-hour intervals. Seven days after vagotomy, plasma glucose and insulin were measured at the midpoint of each feeding period. In control rats, hepatic vagotomy destroyed circadian rhythms of plasma glucose and insulin probably due to removal of afferent function. In VMH lesioned rats, celiac vagotomy destroyed circadian rhythm of food intake due to the reduction of plasma insulin by removal of efferent function without affecting the loss of circadian rhythms of plasma glucose and insulin.

Effects of chronic stress on food intake in rats: Influence of stressor intensity and duration of daily exposure

The effect of exposure to chronic intermittent stressors of differing intensities [handling, restraint, and immobilization (IMO)] and daily duration (15, 60, and 240 min of IMO) on changes in food intake was studied in adult male rats. Whereas handling did not caused anorexia, restraint slightly reduced food intake and IMO drastically reduced it. The effects were very similar after the 7th and 27th day of exposure to the stressors. Fourteen days of chronic IMO (2 h daily) resulted in decreased food intake as measured on days 1, 10, and 14 of treatment, the inhibition being slightly greater after the first stress session. The circadian rhythm of food intake, expressed as a percent of the total food eaten in a 24 h period, was found to be almost unaffected by chronic IMO, although IMO rats appeared to satiate sooner than control rats. Exposure of rats to chronic IMO (7 days) for 15, 60, and 240 min daily reduced food intake to the same extent in all IMO groups. Taken together, these results suggest that: a) the magnitude of the changes in food intake after chronic exposure to stressors is closely related to their intensity, and b) a severe stressor such as IMO reduces food intake to a certain level that was independent on its daily duration. After repeated exposure to the same stressor, only a slight tendency to recover normal food intake was observed.

Circadian rhythms of food and water intake and urine excretion in diabetic rats

The light/dark (L/D) rhythms of food and water intake and urine output were studied in normal and diabetic rats for 7 consecutive days at 4-h intervals. The control rats showed the highest values of these parameters during the dark phase (83.68% food, 68.71% water, and 67.44% urine). The diabetic rats also maintained this nocturnal predominance, although the values were less marked (59.55% food, 55% water, and 56% urine). A circadian rhythm of food ( ø = 3.31 h) and water ( ø = 3.54 h) intake as well as of the volume of urine excreted ( ø = 1.10) was detected in the control animals. The diabetic rats, in spite of presenting polyphagia, maintain the circadian rhythm of food intake, whereas a loss of the normal circadian variation of drinking intake was observed as well as the absence of circadian rhythm in urinary excretion. It was concluded that in streptozotocin-diabetic rats we have observed a loss of the normal patterns of water intake and urinary excretion, perhaps masked by the polydipsia and polyuria, whereas the circadian rhythm of food intake remains.

Role of intrahypothalamic insulin in circadian patterns of food intake, activity, and body temperature.

These experiments examined the extent to which chronic intrahypothalamic (IH) insulin infusions that alter circadian patterns of food intake (FI) affect the regulation of other diurnally varying behavior in the rat. One-week IH insulin infusion (1.5 microU/hr) significantly decreases rats' night FI and increases day FI but does not alter the diurnal pattern of activity. Mean daily core temperature increased slightly but significantly during insulin infusion, the daily peak of the body temperature rhythm did not shift significantly, and the daily range of body temperature increased. IH insulin infusion in rats living in constant light and thus without circadian rhythm of FI led to significant decreases in FI and body weight. These data support the conclusion that IH insulin infusion alters food intake and body weight through a specific effect on a neural system that regulates food intake and body weight, and not by altering circadian rhythms.