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Review
. 2022 Dec 10;11(24):3996.
doi: 10.3390/cells11243996.

Nutraceuticals in Brown Adipose Tissue Activation

Andrea Armani  1   2 , Alessandra Feraco  1   2 , Elisabetta Camajani  1   3 , Stefania Gorini  1   2 , Mauro Lombardo  1 , Massimiliano Caprio  1   2
Affiliations
Review

Nutraceuticals in Brown Adipose Tissue Activation

Andrea Armani et al. Cells. .

Abstract

Obesity and its associated comorbidities have become pandemic, and challenge the global healthcare system. Lifestyle changes, nutritional interventions and phamaceuticals should be differently combined in a personalized strategy to tackle such a public health burden. Altered brown adipose tissue (BAT) function contributes to the pathophysiology of obesity and glucose metabolism dysfunctions. BAT thermogenic activity burns glucose and fatty acids to produce heat through uncoupled respiration, and can dissipate the excessive calorie intake, reduce glycemia and circulate fatty acids released from white adipose tissue. Thus, BAT activity is expected to contribute to whole body energy homeostasis and protect against obesity, diabetes and alterations in lipid profile. To date, pharmacological therapies aimed at activating brown fat have failed in clinical trials, due to cardiovascular side effects or scarce efficacy. On the other hand, several studies have identified plant-derived chemical compounds capable of stimulating BAT thermogenesis in animal models, suggesting the translational applications of dietary supplements to fight adipose tissue dysfunctions. This review describes several nutraceuticals with thermogenic properties and provides indications, at a molecular level, of the regulation of the adipocyte thermogenesis by the mentioned phytochemicals.

Keywords: brown adipocyte; metabolic syndrome; microbiota; obesity; phytochemicals; thermogenesis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Molecular pathways regulating brown/beige adipocyte differentiation. Cooperation of PPARγ with C/EBPs is crucial for an optimal differentiation. PRDM16 promotes a thermogenic program thorugh interaction with C/EBPs and PPARγ, and loss of PRDM16 results in defective BAT formation. SIRT1 has been shown to deacetylate PPARγ. SIRT1-mediated deacetylation of PPARγ stimulates its interaction with PRDM16, leading to increased expression of brown and beige fat-specific genes. SIRT1 has also been shown to activate AMPK, a key enzyme involved in energy homeostasis. Activation of AMPK contributes to mitochodrial function by regulating the process of mitophagy, and stimulates ATGL activity to increase lipolysis. β-adrenergic receptor activation also stimulates lipolysis, with subsequent release of free fatty acids which promote mitochondrial β-oxidation and direct activation of UCP1.
Figure 2
Figure 2
Schematic representation of the molecur targets involved in brown/beige adipocyte thermogenesis, which are regulated by nutraceuticals. UCP1 function of brown/beige adipocytes is activated by capsinoids, catechins, ephedrine and synephrin via stimulation of the sympathetic nervous system (SNS). Other phytochemicals such as quercetin, resveratrol, isoflavones and berberin directly promote the activation of factors (i.e., PPARγ, AMPK, PRDM16) which increase UCP1 function and expression. Adipocyte AMPK is also activated by capsinoids. Both resveratrol and quercetin have been shown to affect gut microbiota function, resulting in increased production of SCFAs which stimulate UCP1-dependent thermogenesis. Of note, the isoflavone genistein has been shown to increase the circulating levels of the myokine irisin which, in the adipose tissue, induces expression of thermogenic genes, including UCP1.
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Grants and funding

This study was supported by the Italian Ministry of Health (Ricerca Corrente), and by MIUR (Progetti di Ricerca di Interesse Nazionale 2017- project code 2017A5TXC3 – to M.C., Work Package Leader. Figures generation has been performed by using BioRender program.

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