Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue

Wankhade, Umesh D.; Shen, Michael; Yadav, Hariom; Thakali, Keshari

doi:10.1155/2016/2365609

Cited by 69 publications

(64 citation statements)

References 111 publications

(116 reference statements)

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“…The finding that active BAT can be found in cold-exposed adult humans has increased scientific interest in its therapeutic potential to counter diabetes and obesity (Hany et al, 2002;Nedergaard et al, 2007;Saito et al, 2009;van Marken Lichtenbelt et al, 2009;Virtanen et al, 2009). In fact, pharmacological and genetic activation of UCP1 in rodents has been shown to protect them from diet-induced obesity (DIO) (Liu et al, 2003;Poher et al, 2015;Wankhade et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism

et al. 2020

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Section: Introductionmentioning

confidence: 99%

A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism

et al. 2020

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“…BAT uses FFAs released by lipolysis, and CPT1 is essential for the delivery of FFAs into mitochondria [27]. BAT and browned WAT adipocytes are characterized by UCP1 expression and consume energy by oxidizing FFAs inefficiently in mitochondria; therefore, the change from a WATto a BAT-like phenotype is associated with an increase in body temperature [28].…”

Section: Ese Promotes Browning In the Wat Of Hfd-induced Obese Mice Amentioning

confidence: 99%

Ecklonia stolonifera Extract Suppresses Lipid Accumulation by Promoting Lipolysis and Adipose Browning in High-Fat Diet-Induced Obese Male Mice

Jin

Lee

Chei

et al. 2020

Cells

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Obesity develops due to an energy imbalance and manifests as the storage of excess triglyceride (TG) in white adipose tissue (WAT). Recent studies have determined that edible natural materials can reduce lipid accumulation and promote browning in WAT. We aimed to determine whether Ecklonia stolonifera extract (ESE) would increase the energy expenditure in high-fat diet (HFD)-induced obese mice and 3T3-L1 cells by upregulating lipolysis and browning. ESE is an edible brown marine alga that belongs to the family Laminariaceae and contains dieckol, a phlorotannin. We report that ESE inhibits body mass gain by regulating the expression of proteins involved in adipogenesis and lipogenesis. In addition, ESE activates protein kinase A (PKA) and increases the expression of lipolytic enzymes including adipose triglyceride lipase (ATGL), phosphorylated hormone-sensitive lipase (p-HSL), and monoacylglycerol lipase (MGL) and also thermogenic genes, such as carnitine palmitoyltransferase 1 (CPT1), PR domain-containing 16 (PRDM16), and uncoupling protein 1 (UCP1). These findings indicate that ESE may represent a promising natural means of preventing obesity and obesity-related metabolic diseases.

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“…Luckily, alternative ways of activating the endogenous BAT are available. Among drugs capable of inducing such browning is CL 316243, an agonist of the β3 adrenergic receptor, which not only promotes BAT activity but also protects against WAT hyperplasia in the early stages of obesity (Wankhade et al 2016). The TZD-derived partial PPARγ agonist GQ-16 decreased weight gain in spite of higher energy intake, reduced fat mass and liver TG content and increased morphological and molecular markers of BAT activation in male high-fat diet-fed Swiss mice (Coelho et al 2016).…”

Section: Clinical Perspectives and Potential Therapeutic Applicationsmentioning

confidence: 99%

Mitochondrial oxidative stress in obesity: role of the mineralocorticoid receptor

Lefranc

Friederich‐Persson

Palacios

et al. 2018

Journal of Endocrinology

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Obesity is a multifaceted, chronic, low-grade inflammation disease characterized by excess accumulation of dysfunctional adipose tissue. It is often associated with the development of cardiovascular (CV) disorders, insulin resistance and diabetes. Under pathological conditions like in obesity, adipose tissue secretes bioactive molecules called 'adipokines', including cytokines, hormones and reactive oxygen species (ROS). There is evidence suggesting that oxidative stress, in particular, the ROS imbalance in adipose tissue, may be the mechanistic link between obesity and its associated CV and metabolic complications. Mitochondria in adipose tissue are an important source of ROS and their dysfunction contributes to the pathogenesis of obesity-related type 2 diabetes. Mitochondrial function is regulated by several factors in order to preserve mitochondria integrity and dynamics. Moreover, the renin-angiotensin-aldosterone system is over-activated in obesity. In this review, we focus on the pathophysiological role of the mineralocorticoid receptor in the adipose tissue and its contribution to obesity-associated metabolic and CV complications. More specifically, we discuss whether dysregulation of the mineralocorticoid system within the adipose tissue may be the upstream mechanism and one of the early events in the development of obesity, via induction of oxidative stress and mitochondrial dysfunction, thus impacting on systemic metabolism and the CV system.

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Novel Browning Agents, Mechanisms, and Therapeutic Potentials of Brown Adipose Tissue

Cited by 69 publications

References 111 publications

A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism

A Genetic Model to Study the Contribution of Brown and Brite Adipocytes to Metabolism

Ecklonia stolonifera Extract Suppresses Lipid Accumulation by Promoting Lipolysis and Adipose Browning in High-Fat Diet-Induced Obese Male Mice

Mitochondrial oxidative stress in obesity: role of the mineralocorticoid receptor

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