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  1. Ismail S, Manaf RA, Mahmud A
    East Mediterr Health J, 2019 Jun 04;25(4):239-245.
    PMID: 31210344 DOI: 10.26719/emhj.19.011
    Background: Research on the health benefits of fasting is growing; this includes time-restricted feeding and Islamic fasting.

    Aims: This article aims to review and highlight the similarities and differences between time-restricted feeding and Islamic fasting during Ramadan.

    Methods: A scoping review was undertaken to identify relevant articles that answered the research question: what are the similarities and differences in characteristics of time-restricted feeding and Islamic fasting? MEDLINE/PubMed was searched using the terms: time-restricted feeding, and weight. Inclusion criteria were: original research and review articles; written in English; and published between the years 2000 and 2017.

    Results: A total of 25 articles that answered the research question were included in the review: 15 original research papers and 10 reviews. The findings suggest that Ramadan fasting is a form of time-restricted feeding in the contemporary context because of the period when eating is not allowed. The fasting duration reported in time-restricted feeding ranged from 4 to 24 hours, which is longer than that of Islamic fasting which is between 8 and 20 hours. Both time-restricted feeding and Islamic fasting have been found to have positive health effects, including weight reduction.

    Conclusion: Time-restricted feeding and Islamic fasting have many similar characteristics and reported positive health effects.

    Matched MeSH terms: Adipose Tissue/physiopathology
  2. Yong VW, Tan YJ, Ng YD, Choo XY, Sugumaran K, Chinna K, et al.
    Parkinsonism Relat Disord, 2020 08;77:28-35.
    PMID: 32615497 DOI: 10.1016/j.parkreldis.2020.06.015
    INTRODUCTION: Although weight loss is common in Parkinson's disease (PD), longitudinal studies assessing weight and body composition changes are limited.

    METHODS: In this three-year longitudinal study, 125 subjects (77 PD patients and 48 spousal/sibling controls) underwent clinical, biochemical and body composition assessments using dual-energy X-ray absorptiometry.

    RESULTS: Patients were older than controls (65.6 ± 8.9 vs. 62.6 ± 7.1, P = 0.049), with no significant differences in gender, comorbidities, dietary intake and physical activity. Clinically significant weight loss (≥5% from baseline weight) was recorded in 41.6% of patients, with a doubling of cases (6.5 to 13.0%) classified as underweight at study end. Over three years, patients demonstrated greater reductions in BMI (mean -1.2 kg/m2, 95%CI-2.0 to -0.4), whole-body fat percentage (-2.5% points, 95%CI-3.9 to -1.0), fat mass index (FMI) (-0.9 kg/m2, 95%CI-1.4 to -0.4), visceral fat mass (-0.1 kg, 95%CI-0.2 to 0.0), and subcutaneous fat mass (-1.9 kg, 95%CI-3.4 to -0.5) than in controls, with significant group-by-time interactions after adjusting for age and gender. Notably, 31.2% and 53.3% of patients had FMI<3rd (severe fat deficit) and <10th centiles, respectively. Muscle mass indices decreased over time in both groups, without significant group-by-time interactions. Multiple linear regression models showed that loss of body weight and fat mass in patients were associated with age, dyskinesia, psychosis and constipation.

    CONCLUSIONS: We found progressive loss of weight in PD patients, with greater loss of both visceral and subcutaneous fat, but not muscle, compared to controls. Several associated factors (motor and non-motor disease features) were identified for these changes, providing insights on possible mechanisms and therapeutic targets.

    Matched MeSH terms: Adipose Tissue/physiopathology*
  3. Cheng CK, Bakar HA, Gollasch M, Huang Y
    Cardiovasc Drugs Ther, 2018 10;32(5):481-502.
    PMID: 30171461 DOI: 10.1007/s10557-018-6820-z
    Perivascular adipose tissue (PVAT) refers to the local aggregate of adipose tissue surrounding the vascular tree, exhibiting phenotypes from white to brown and beige adipocytes. Although PVAT has long been regarded as simply a structural unit providing mechanical support to vasculature, it is now gaining reputation as an integral endocrine/paracrine component, in addition to the well-established modulator endothelium, in regulating vascular tone. Since the discovery of anti-contractile effect of PVAT in 1991, the use of multiple rodent models of reduced amounts of PVAT has revealed its regulatory role in vascular remodeling and cardiovascular implications, including atherosclerosis. PVAT does not only release PVAT-derived relaxing factors (PVRFs) to activate multiple subsets of endothelial and vascular smooth muscle potassium channels and anti-inflammatory signals in the vasculature, but it does also provide an interface for neuron-adipocyte interactions in the vascular wall to regulate arterial vascular tone. In this review, we outline our current understanding towards PVAT and attempt to provide hints about future studies that can sharpen the therapeutic potential of PVAT against cardiovascular diseases and their complications.
    Matched MeSH terms: Adipose Tissue/physiopathology
  4. Abu Bakar MH, Shariff KA, Tan JS, Lee LK
    Eur J Pharmacol, 2020 Sep 15;883:173371.
    PMID: 32712089 DOI: 10.1016/j.ejphar.2020.173371
    Accumulating evidence indicates that adipose tissue inflammation and mitochondrial dysfunction in skeletal muscle are inextricably linked to obesity and insulin resistance. Celastrol, a bioactive compound derived from the root of Tripterygium wilfordii exhibits a number of attributive properties to attenuate metabolic dysfunction in various cellular and animal disease models. However, the underlying therapeutic mechanisms of celastrol in the obesogenic environment in vivo remain elusive. Therefore, the current study investigated the metabolic effects of celastrol on insulin sensitivity, inflammatory response in adipose tissue and mitochondrial functions in skeletal muscle of the high fat diet (HFD)-induced obese rats. Our study revealed that celastrol supplementation at 3 mg/kg/day for 8 weeks significantly reduced the final body weight and enhanced insulin sensitivity of the HFD-fed rats. Celastrol noticeably improved insulin-stimulated glucose uptake activity and increased expression of plasma membrane GLUT4 protein in skeletal muscle. Moreover, celastrol-treated HFD-fed rats showed attenuated inflammatory responses via decreased NF-κB activity and diminished mRNA expression responsible for classically activated macrophage (M1) polarization in adipose tissues. Significant improvement of muscle mitochondrial functions and enhanced antioxidant defense machinery via restoration of mitochondrial complexes I + III linked activity were effectively exhibited by celastrol treatment. Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. Together, these results further demonstrate heretofore the conceivable therapeutic mechanisms of celastrol in vivo against HFD-induced obesity mediated through attenuation of inflammatory response in adipose tissue and enhanced mitochondrial functions in skeletal muscle.
    Matched MeSH terms: Adipose Tissue/physiopathology
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