Mitochondria in White, Brown, and Beige Adipocytes

Čedíková, Miroslava; Kripnerová, Michaela; Dvořáková, Jana; Pitule, Pavel; Grundmanova, Martina; Babuška, Václav; Müllerová, Dana; Kuncová, Jitka

doi:10.1155/2016/6067349

Cited by 182 publications

(168 citation statements)

References 127 publications

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“…Beiging is associated with an increase in mitochondrial density 28, 29 . We used the PhAM excised mouse, in which a fluorescent protein from the octocoral Dendronephthya , Dendra2, is fused to a Cox8 mitochondrial targeting signal, yielding mito-Dendra2 (Fig.…”

Section: Fsh Ab Triggers Beiging Of White Adipocytesmentioning

confidence: 99%

Blocking FSH induces thermogenic adipose tissue and reduces body fat

Liu

Yuen

et al. 2017

Nature

269

280

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Menopause is associated with bone loss and enhanced visceral adiposity. We have shown previously that a polyclonal antibody (Ab) to the β-subunit of the pituitary hormone Fsh increases bone mass in mice. Here, we report that this Ab sharply reduces adipose tissue in wild type mice, phenocopying genetic Fshr haploinsufficiency. The Ab also causes profound beiging, increases cellular mitochondrial density, activates brown adipose tissue, and enhances thermogenesis. These actions result from the specific binding of Ab to Fshβ to block its action. Our studies uncover novel opportunities for co-treating obesity and osteoporosis.

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Section: Fsh Ab Triggers Beiging Of White Adipocytesmentioning

confidence: 99%

Blocking FSH induces thermogenic adipose tissue and reduces body fat

Liu

Yuen

et al. 2017

Nature

269

280

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“…Mitochondria are multifunctional organelles. They contribute to cellular calcium homeostasis, trigger apoptosis, and regulate cellular metabolism [5,6,7,8]. However, the primary function of mitochondria is to generate ATP to power cells.…”

Section: Introductionmentioning

confidence: 99%

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Tan

Manchester

Qin

et al. 2016

IJMS

312

256

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Melatonin has been speculated to be mainly synthesized by mitochondria. This speculation is supported by the recent discovery that aralkylamine N-acetyltransferase/serotonin N-acetyltransferase (AANAT/SNAT) is localized in mitochondria of oocytes and the isolated mitochondria generate melatonin. We have also speculated that melatonin is a mitochondria-targeted antioxidant. It accumulates in mitochondria with high concentration against a concentration gradient. This is probably achieved by an active transportation via mitochondrial melatonin transporter(s). Melatonin protects mitochondria by scavenging reactive oxygen species (ROS), inhibiting the mitochondrial permeability transition pore (MPTP), and activating uncoupling proteins (UCPs). Thus, melatonin maintains the optimal mitochondrial membrane potential and preserves mitochondrial functions. In addition, mitochondrial biogenesis and dynamics is also regulated by melatonin. In most cases, melatonin reduces mitochondrial fission and elevates their fusion. Mitochondrial dynamics exhibit an oscillatory pattern which matches the melatonin circadian secretory rhythm in pinealeocytes and probably in other cells. Recently, melatonin has been found to promote mitophagy and improve homeostasis of mitochondria.

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“…However, the heterogeneity of fat composition [white ( WAT ), brown ( BAT ) and beige/brite/brown-like ( bAT ) adipose tissues] and the distribution of these depots, can be more crucial for the development of cardiometabolic disruptions [4, 5]. In physiological conditions, the presence of WAT and BAT in various stores of adipose tissue suggests a direct transformation of differentiated pre-adipocytes (Myf5 − and Myf5 + , for WAT and BAT , respectively) into mature cells with different morphological and functional characteristics according with location [6].…”

Section: Fat Distribution and Compositionmentioning

confidence: 99%

“…In general, WAT accumulates excess of energy as single lipid droplets of triglycerides (TAG) within its adipocytes, which express high levels of leptin and exhibit a few variable number of mitochondria (Table 1). WAT weight generally represents as much as 20% of body weight on normal adults and primarily acts as a storage site for fat, preserving supplementary calories for use in times of scarcity [5]. On the other hand, BAT can store lipids in multiple small vacuole inside its smaller multi mitochondrial brown adipocytes.…”

Section: Fat Distribution and Compositionmentioning

confidence: 99%

Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes

González

Moreno-Villegas

González-Bris

et al. 2017

Cardiovasc Diabetol

157

131

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Nowadays, obesity is seriously increasing in most of the populations all over the world, and is associated with the development and progression of high-mortality diseases such as type-2 diabetes mellitus (T2DM) and its subsequent cardiovascular pathologies. Recent data suggest that both body fat distribution and adipocyte phenotype, can be more determinant for fatal outcomes in obese patients than increased general adiposity. In particular, visceral adiposity is significantly linked to long term alterations on different cardiac structures, and in developed forms of myocardial diseases such as hypertensive and ischaemic heart diseases, and diabetic cardiomyopathy. Interestingly, this depot may be also related to epicardial fat accumulation through secretion of lipids, adipokines, and pro-inflammatory and oxidative factors from adipocytes. Thus, visceral adiposity and its white single-lipid-like adipocytes, are risk factors for different forms of heart disease and heart failure, mainly in higher degree obese subjects. However, under specific stimuli, some of these adipocytes can transdifferentiate to brown multi-mitochondrial-like adipocytes with anti-inflammatory and anti-apoptotic proprieties. Accordingly, in order to improve potential cardiovascular abnormalities in obese and T2DM patients, several therapeutic strategies have been addressed to modulate the visceral and epicardial fat volume and phenotypes. In addition to lifestyle modifications, specific genetic manipulations in adipose tissue and administration of PPARγ agonists or statins, have improved fat volume and phenotype, and cardiovascular failures. Furthermore, incretin stimulation reduced visceral and epicardial fat thickness whereas increased formation of brown adipocytes, alleviating insulin resistance and associated cardiovascular pathologies.

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Mitochondria in White, Brown, and Beige Adipocytes

Cited by 182 publications

References 127 publications

Blocking FSH induces thermogenic adipose tissue and reduces body fat

Blocking FSH induces thermogenic adipose tissue and reduces body fat

Melatonin: A Mitochondrial Targeting Molecule Involving Mitochondrial Protection and Dynamics

Regulation of visceral and epicardial adipose tissue for preventing cardiovascular injuries associated to obesity and diabetes

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