Nurrani Mustika Dewi
Prodia Clinical Laboratory, Jl. Cisangkuy No.2, Bandung

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Chronodisruption and Obesity Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 7, No 3 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i3.184

Abstract

BACKGROUND: Attempts to understand the causes of obesity and develop new therapeutic strategies have mostly focused on caloric intake and energy expenditure. Recent studies have shown that the circadian clock controls energy homeostasis by regulating circadian expression and/or activity of enzymes, hormones, and transport systems involved in metabolism. Moreover, disruption of circadian rhythms leads to obesity and metabolic disorders.CONTENT:Regularly alternating periods of light and darkness, such as normally occur with the rising and the setting of the sun, are essential for the maintenance of undisturbed circadian rhythms in all organisms including humans. The light-dark environment, as detected by specialized photoreceptors in the retinas, impacts the endogenous circadian clock in the anterior hypothalamus, the suprachiasmatic nuclei. These nuclei, via both neural and humoral signals, communicate with cells throughout the organism to establish regular circadian rhythms. The introduction of artificial sources of light roughly 150 years ago has significantly undermined the naturally occurring light-dark environment and, likewise, has disturbed circadian rhythms since light is now available at unusual times, i.e., at night. Light at night is known to cause circadian disruption and melatonin suppression. Many potentially pathophysiological consequences of these artificial light-mediated changes, include cancer, cardiovascular diseases, insomnia, metabolic syndrome, diabetes, and cognitive disorders may be aggravated by the increased exposure to light at night, which is inevitable in well-developed societies that have undergone extensive electrification.SUMMARY: Therefore, it is plausible that resetting of the circadian clock can be used as a new approach to attenuate obesity. Feeding regimens, such as restricted feeding, calorie restriction and intermittent fasting, provide a time cue and reset the circadian clock and lead to better health. In contrast, high-fat diet leads to disrupted circadian expression of metabolic factors and obesity.KEYWORDS: obesity, circadian clock, metabolism, chronodisruption
Adipose Tissue, Inflammation (Meta-inflammation) and Obesity Management Anna Meiliana; Nurrani Mustika Dewi; Andi Wijaya
The Indonesian Biomedical Journal Vol 7, No 3 (2015)
Publisher : The Prodia Education and Research Institute (PERI)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.18585/inabj.v7i3.185

Abstract

BACKGROUND: Obesity-induced inflammation contributes to the development of type 2 diabetes, metabolic syndrome, and cardiovascular disease.CONTENT:The last decade has seen a sharp increase in our appreciation for the macrophage as a critical regulator of metabolic status in obesity. Activation of adipose tissue (AT) macrophages within fat depots is coupled with the development of obesity-induced proinflammatory state and insulin resistance (IR). The activation of classically activated M1 macrophages at the expense of anti-inflammatory M2 macrophages has been causally linked to the development of AT inflammation and metabolic syndrome, a pathophysiological state aptly termed as ‘metainflammation’. It is recognized that several proinflammatory cytokines, including interleukin (IL)-1β, are implicated in disrupting insulin signaling. Our developing appreciation of links among obesity, inflammation and cardiovascular disease will require multiple complementary approaches to leverage new concepts into translatable outcomes. Careful characterization of human patients, particularly analysis of AT distribution, will be needed to stratify subjects that are most likely obese/metabolically healthy from those that are obese/metabolically unhealthy.SUMMARY: It has been suggested that individuals with the condition known as metabolically healthy obese (MHO) may not have the same increased risk for the development of metabolic abnormalities as their non-metabolically healthy counterparts. A complications-centric model for the medical management of obesity emphasizes the identification and staging of complications, and treatment paradigm directed at patients who would gain the most benefit from weight loss.KEYWORDS: obesity, inflammation, insulin resistance, M1/M2 macrophage.