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Chronic L-menthol-induced browning of white adipose tissue hypothesis: A putative therapeutic regime for combating obesity and improving metabolic health

Sakellariou, P. (författare)
Valente, A. (författare)
Carrillo, A. E. (författare)
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Metsios, G. S. (författare)
Nadolnik, L. (författare)
Jamurtas, A. Z. (författare)
Koutedakis, Y. (författare)
Boguszewski, C. (författare)
Andrade, C. M. B. (författare)
Svensson, Per-Arne, 1969 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine
Kawashita, N. H. (författare)
Flouris, A. D. (författare)
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 (creator_code:org_t)
Elsevier BV, 2016
2016
Engelska.
Ingår i: Medical Hypotheses. - : Elsevier BV. - 0306-9877. ; 93, s. 21-26
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • Introduction: Obesity constitutes a serious global health concern reaching pandemic prevalence rates. The existence of functional brown adipose tissue (BAT) in adult humans has provoked intense research interest in the role of this metabolically active tissue in whole-body energy balance and body weight regulation. A number of environmental, physiological, pathological, and pharmacological stimuli have been proposed to induce BAT-mediated thermogenesis and functional thermogenic BAT-like activity in white adipose tissue (WAT), opening new avenues for therapeutic strategies based on enhancing the number of beige adipocytes in WAT. Hypothesis: Recent evidence support a role of L-menthol cooling, mediated by TRPM8 receptor, on UCP1-dependent thermogenesis and BAT-like activity in classical WAT depots along with the recruitment of BAT at specific anatomical sites. L-Menthol-induced BAT thermogenesis has been suggested to occur by a beta-adrenergic-independent mechanism, avoiding potential side-effects due to extensive beta-adrenergic stimulation mediated by available beta receptor agonists. L-Menthol has been also linked to the activation of the cold-gated ion channel TRPA1. However, its role in L-menthol-induced UCP1-dependent thermogenic activity in BAT and WAT remains undetermined. White adipose tissue plasticity has important clinical implications for obesity prevention and/or treatment because higher levels of UCP1-dependent thermogenesis can lead to enhanced energy expenditure at a considerable extent. We hypothesize that chronic dietary L-menthol treatment could induce TRPM8- and TRPA1-dependent WAT adaptations, resembling BAT-like activity, and overall improve whole-body metabolic health in obese and overweight individuals. Conclusions: The putative impact of chronic L-menthol dietary treatment on the stimulation of BAT-like activity in classical WAT depots in humans remains unknown. A detailed experimental design has been proposed to investigate the hypothesized L-menthol-induced browning of WAT. If our hypothesis was to be confirmed, TRPM8/TRPA1-induced metabolic adaptations of WAT to BAT-like activity could provide a promising novel therapeutic approach for increasing energy expenditure, regulating body weight, and preventing obesity and its related co-morbidities in humans. (C) 2016 Elsevier Ltd. All rights reserved.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Endokrinologi och diabetes (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Endocrinology and Diabetes (hsv//eng)

Nyckelord

L-Menthol
UCP1
TRPM8
TRPA1
White adipose tissue
Brown adipose tissue
Obesity
Overweight
ppar-gamma activation
trp channels
mitochondrial biogenesis
molecular
determinant
energy-expenditure
gene-expression
fat development
messenger-rna
beige fat
cold

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