Significance and application of melatonin - relation to human obesity

[cvictorg]

Significance and application of melatonin in the r... [Obes Rev. 2011] - PubMed result

Obes Rev. 2011 Mar;12(3):167-88. doi: 10.1111/j.1467-789X.2010.00756.x.
Significance and application of melatonin in the regulation of brown adipose tissue metabolism: relation to human obesity.
Tan DX, Manchester LC, Fuentes-Broto L, Paredes SD, Reiter RJ.

Department of Cellular and Structural Biology, the University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Abstract
A worldwide increase in the incidence of obesity indicates the unsuccessful battle against this disorder. Obesity and the associated health problems urgently require effective strategies of treatment. The new discovery that a substantial amount of functional brown adipose tissue (BAT) is retained in adult humans provides a potential target for treatment of human obesity. BAT is active metabolically and disposes of extra energy via generation of heat through uncoupling oxidative phosphorylation in mitochondria. The physiology of BAT is readily regulated by melatonin, which not only increases recruitment of brown adipocytes but also elevates their metabolic activity in mammals. It is speculated that the hypertrophic effect and functional activation of BAT induced by melatonin may likely apply to the human. Thus, melatonin, a naturally occurring substance with no reported toxicity, may serve as a novel approach for treatment of obesity. Conversely, because of the availability of artificial light sources, excessive light exposure after darkness onset in modern societies should be considered a potential contributory factor to human obesity as light at night dramatically reduces endogenous melatonin production. In the current article, the potential associations of melatonin, BAT, obesity and the medical implications are discussed.

Melatonin and circadian biology in human cardiovas... [J Pineal Res. 2010] - PubMed result

J Pineal Res. 2010 Aug;49(1):14-22. Epub 2010 Jun 1.
Melatonin and circadian biology in human cardiovascular disease.
Dominguez-Rodriguez A, Abreu-Gonzalez P, Sanchez-Sanchez JJ, Kaski JC, Reiter RJ.

Department of Cardiology, Hospital Universitario de Canarias, Tenerife, Spain. adrvdg@hotmail.com
Abstract
Diurnal rhythms influence cardiovascular physiology, i.e. heart rate and blood pressure, and they appear to also modulate the incidence of serious adverse cardiac events. Diurnal variations occur also at the molecular level including changes in gene expression in the heart and blood vessels. Moreover, the risk/benefit ratio of some therapeutic strategies and the concentration of circulating cardiovascular system biomarkers may also vary across the 24-hr light/dark cycle. Synchrony between external and internal diurnal rhythms and harmony among molecular rhythms within the cell are essential for normal organ biology. Diurnal variations in the responsiveness of the cardiovascular system to environmental stimuli are mediated by a complex interplay between extracellular (i.e. neurohumoral factors) and intracellular (i.e. specific genes that are differentially light/dark regulated) mechanisms. Neurohormones, which are particularly relevant to the cardiovascular system, such as melatonin, exhibit a diurnal variation and may play a role in the synchronization of molecular circadian clocks in the peripheral tissue and the suprachiasmatic nucleus. Moreover, mounting evidence reveals that the blood melatonin rhythm has a crucial role in several cardiovascular functions, including daily variations in blood pressure. Melatonin has antioxidant, anti-inflammatory, chronobiotic and, possibly, epigenetic regulatory functions. This article reviews current knowledge related to the biological role of melatonin and its circadian rhythm in cardiovascular disease.

http://www.heartandmetabolism.org/pdf/44/3.pdf

Disruption of normal circadian rhythms and cardiovascular events

Abstract
The intrinsic properties of the heart and the vascular tree exhibit marked oscillations over 24 h. Diurnal variations in the response of the cardiovascular system to environmental stimuli are mediated by the complex interplay of extracellular (ie, neurohumoral factors) and intracellular (ie, circadian clock) in?uences. The intracellular circadian clock comprises a series of transcriptional modulators that together allow the cell to ‘‘perceive’’ the time of day, thus enabling suitable responses to expected stimuli. These molecular timepieces have been identi?ed and characterized within both vascular smooth muscle cells and cardiomyocytes, giving rise to a multitude of hypotheses regarding the potential role of the circadian clock as a modulator of physiological and pathophysiological cardiovascular events. This article summarizes the evidence available at present linking circadian rhythm disruption
and cardiovascular disease.

 

[cvictorg]

Insufficient sleep undermines dietary efforts to r... [Ann Intern Med. 2010] - PubMed result

Insufficient Sleep Undermines Dietary Efforts to Reduce Adiposity

Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD.

The University of Chicago, Illinois, USA.
Comment in:

Ann Intern Med. 2010 Oct 5;153(7):475-6.
Summary for patients in:

Ann Intern Med. 2010 Oct 5;153(7):I28.
Abstract
BACKGROUND: Sleep loss can modify energy intake and expenditure.

OBJECTIVE: To determine whether sleep restriction attenuates the effect of a reduced-calorie diet on excess adiposity.

DESIGN: Randomized, 2-period, 2-condition crossover study.

SETTING: University clinical research center and sleep laboratory.

PATIENTS: 10 overweight nonsmoking adults (3 women and 7 men) with a mean age of 41 years (SD, 5) and a mean body mass index of 27.4 kg/m² (SD, 2.0).

INTERVENTION: 14 days of moderate caloric restriction with 8.5 or 5.5 hours of nighttime sleep opportunity.

MEASUREMENTS: The primary measure was loss of fat and fat-free body mass. Secondary measures were changes in substrate utilization, energy expenditure, hunger, and 24-hour metabolic hormone concentrations.

RESULTS: Sleep curtailment decreased the proportion of weight lost as fat by 55% (1.4 vs. 0.6 kg with 8.5 vs. 5.5 hours of sleep opportunity, respectively; P = 0.043) and increased the loss of fat-free body mass by 60% (1.5 vs. 2.4 kg; P = 0.002). This was accompanied by markers of enhanced neuroendocrine adaptation to caloric restriction, increased hunger, and a shift in relative substrate utilization toward oxidation of less fat.

LIMITATION: The nature of the study limited its duration and sample size.

CONCLUSION: The amount of human sleep contributes to the maintenance of fat-free body mass at times of decreased energy intake. Lack of sufficient sleep may compromise the efficacy of typical dietary interventions for weight loss and related metabolic risk reduction.

PRIMARY FUNDING SOURCE: National Institutes of Health.


From the full study - see link

In summary, exposure of overweight middle-aged adults to 2 weeks of combined energy and sleep restriction produced a catabolic state characterized by reduced loss of body fat and increased loss of fat-free body mass, accompanied by increased hunger and changes in energy expenditure and the neuroendocrine control of substrate utilization. These results highlight the importance of human sleep for maintenance of fat-free body mass during periods of reduced energy intake and suggest that insuf?cient sleep may compromise several factors that contribute to the ef?cacy of and adherence to dietary energy-restriction strategies for metabolic risk reduction.