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      Circadian Rhythm Profiles in Women with Night Eating Syndrome

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          Abstract

          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.

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          Most cited references30

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          Stomach is a major source of circulating ghrelin, and feeding state determines plasma ghrelin-like immunoreactivity levels in humans.

          Ghrelin, an endogenous ligand for the GH secretagogue receptor, was isolated from rat stomach and is involved in a novel system for regulating GH release. Although previous studies in rodents suggest that ghrelin is also involved in energy homeostasis and that ghrelin secretion is influenced by feeding, little is known about plasma ghrelin in humans. To address this issue, we studied plasma ghrelin-like immunoreactivity levels and elucidated the source of circulating ghrelin and the effects of feeding state on plasma ghrelin-like immunoreactivity levels in humans. The plasma ghrelin-like immunoreactivity concentration in normal humans measured by a specific RIA was 166.0 +/- 10.1 fmol/ml. Northern blot analysis of various human tissues identified ghrelin mRNA found most abundantly in the stomach and plasma ghrelin-like immunoreactivity levels in totally gastrectomized patients were reduced to 35% of those in normal controls. Plasma ghrelin-like immunoreactivity levels were increased by 31% after 12-h fasting and reduced by 22% immediately after habitual feeding. In patients with anorexia nervosa, plasma ghrelin-like immunoreactivity levels were markedly elevated compared with those in normal controls (401.2 +/- 58.4 vs. 192.8 +/- 19.4 fmol/ml) and were negatively correlated with body mass indexes. We conclude that the stomach is a major source of circulating ghrelin and that plasma ghrelin-like immunoreactivity levels reflect acute and chronic feeding states in humans.
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            A human phase-response curve to light.

            Using 'classical' experimental protocols, a human phase-response curve (PRC) to a single 3-h bright light pulse has been established. When the light pulse was centred slightly before the time of body temperature minimum, the circadian system delayed, whilst a pulse slightly after the minimum advanced it. Maximum phase shifts were about 2 h. When light pulses over 3 successive cycles were used, larger shifts (4-7 h) were produced. It is concluded that the human PRC does not differ in principle from that found in other species, except with respect to the light intensity required.
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              The relationship between nutrition and circadian rhythms in mammals.

              Oren Froy (2015)
              The master clock located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus regulates circadian rhythms in mammals. The clock is an intracellular, transcriptional mechanism sharing the same molecular components in SCN neurons and in peripheral cells, such as the liver, intestine, and retina. The circadian clock controls food processing and energy homeostasis by regulating the expression and/or activity of enzymes involved in cholesterol, amino acid, lipid, glycogen, and glucose metabolism. In addition, many hormones involved in metabolism, such as insulin, glucagon, adiponectin, corticosterone, leptin, and ghrelin, exhibit circadian oscillation. Furthermore, disruption of circadian rhythms is involved in the development of cancer, metabolic syndrome, and obesity. Metabolism and food intake also feed back to influence the biological clock. Calorie restriction (CR) entrains the SCN clock, whereas timed meals entrain peripheral oscillators. Furthermore, the cellular redox state, dictated by food metabolism, and several nutrients, such as glucose, ethanol, adenosine, caffeine, thiamine, and retinoic acid, can phase-shift circadian rhythms. In conclusion, there is a large body of evidence that links feeding regimens, food components, and the biological clock.
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                Author and article information

                Journal
                Journal of Biological Rhythms
                J Biol Rhythms
                SAGE Publications
                0748-7304
                1552-4531
                February 2009
                February 2009
                February 2009
                February 2009
                : 24
                : 1
                : 85-94
                Affiliations
                [1 ]Division of Sleep and Chronobiology (Psychiatry), University of Pennsylvania School of Medicine, Philadelphia, PA, USA,
                [2 ]Center for Weight and Eating Disorders (Psychiatry), University of Pennsylvania School of Medicine, Philadelphia, PA, USA
                [3 ]Division of Sleep and Chronobiology (Psychiatry), University of Pennsylvania School of Medicine, Philadelphia, PA, USA, Chronobiology and Sleep Group, Brain and Mind Research Institute, University of Sydney, Camperdown, Australia
                [4 ]Division of Sleep and Chronobiology (Psychiatry), University of Pennsylvania School of Medicine, Philadelphia, PA, USA, Sleep and Performance Research Center, Washington State University, Spokane, WA 99210
                [5 ]Division of Endocrinology, Diabetes and Metabolism (Medicine), University of Pennsylvania School of Medicine, Philadelphia, PA, USA
                [6 ]Division of Metabolism, Endocrinology and Nutrition (Medicine), University of Washington, Seattle, WA, USA
                [7 ]Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY, USA
                [8 ]Division of Sleep and Chronobiology (Psychiatry), University of Pennsylvania School of Medicine, Philadelphia, PA, USA
                Article
                10.1177/0748730408328914
                3564642
                19150931
                c857e133-9108-4cd7-829b-6bb60f58372c
                © 2009

                http://journals.sagepub.com/page/policies/text-and-data-mining-license

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