Brain-derived neurotrophic factor modulates mitochondrial dynamics and thermogenic phenotype on 3T3-L1 adipocytes

Colitti, Monica; Montanari, Tommaso

doi:10.1016/j.tice.2020.101388

Cited by 13 publications

(13 citation statements)

References 40 publications

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“…Moreover, chronic activation of BDNF receptor, TrkB, by the non-peptidyl agonist 7,8-dihydroxyflavone (7,8-DHF), increased mitochondrial content in mouse skeletal muscles through activating the AMPK-PGC-1α cascade and alleviated the detrimental effects of diet-induced obesity [56]. BDNF is also able to promote mitochondrial biogenesis in hippocampal neurons [57] and controls mitochondrial dynamics and clearance in adipocytes [58], myocardium [59], motor neurons [60], and retinal cells [61]. Although all these findings suggest that BDNF is a regulator of mitochondrial behavior in a great variety of tissues, it is interesting to note that none of these studies were exercise-related.…”

Section: Brain-derived Neurotrophic Factor (Bdnf)mentioning

confidence: 99%

Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle—Do Myokines Play a Role?

Pang¹,

Chan²,

Chan³

2021

Antioxidants

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Mitochondria are the cellular powerhouses that generate adenosine triphosphate (ATP) to substantiate various biochemical activities. Instead of being a static intracellular structure, they are dynamic organelles that perform constant structural and functional remodeling in response to different metabolic stresses. In situations that require a high ATP supply, new mitochondria are assembled (mitochondrial biogenesis) or formed by fusing the existing mitochondria (mitochondrial fusion) to maximize the oxidative capacity. On the other hand, nutrient overload may produce detrimental metabolites such as reactive oxidative species (ROS) that wreck the organelle, leading to the split of damaged mitochondria (mitofission) for clearance (mitophagy). These vital processes are tightly regulated by a sophisticated quality control system involving energy sensing, intracellular membrane interaction, autophagy, and proteasomal degradation to optimize the number of healthy mitochondria. The effective mitochondrial surveillance is particularly important to skeletal muscle fitness because of its large tissue mass as well as its high metabolic activities for supporting the intensive myofiber contractility. Indeed, the failure of the mitochondrial quality control system in skeletal muscle is associated with diseases such as insulin resistance, aging, and muscle wasting. While the mitochondrial dynamics in cells are believed to be intrinsically controlled by the energy content and nutrient availability, other upstream regulators such as hormonal signals from distal organs or factors generated by the muscle itself may also play a critical role. It is now clear that skeletal muscle actively participates in systemic energy homeostasis via producing hundreds of myokines. Acting either as autocrine/paracrine or circulating hormones to crosstalk with other organs, these secretory myokines regulate a large number of physiological activities including insulin sensitivity, fuel utilization, cell differentiation, and appetite behavior. In this article, we will review the mechanism of myokines in mitochondrial quality control and ROS balance, and discuss their translational potential.

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Section: Brain-derived Neurotrophic Factor (Bdnf)mentioning

confidence: 99%

Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle—Do Myokines Play a Role?

Pang¹,

Chan²,

Chan³

2021

Antioxidants

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“…Although the above studies suggest that mature adipocytes might not produce mBDNF, they do respond to both pro-BDNF and mBDNF stimulations as a significant amount of TrkB and p75NTR could be found in WAT [ 35 , 42 ]. Moreover, more mitochondrial fission and browning were detected in the differentiated 3T3-L1 adipocytes after BDNF stimulation [ 43 ]. It is possible that the non-adipose cells in WAT produce BDNF paracrine to modulate the metabolic activities of their adjacent adipocytes.…”

Section: Bdnf In Adipose Tissuementioning

confidence: 99%

Section: Bdnf In Skeletal Musclementioning

confidence: 99%

“…Hence, the clearance of damaged mitochondria is diminished in the muscle of MBKO mice, leading to the accumulation of dysfunctional mitochondria for efficient FAO, severe insulin resistance, and obesity [28]. It is noteworthy that BDNF-or 7,8-DHF-regulated mitophagy could also be detected in cultured cardiomyocytes, adipocytes, retinal ganglion, and vascular endothelial cells, but whether AMPK in these cells is involved in the process remains to be determined [43,[103][104][105] In addition to muscle [88,106], BDNF has a significant role in regulating the mitochondrial respiration in other tissues. For instance, mBDNF or 7,8-DHF augments the mitochondrial respiration in neuron preparation [107], injured cortical neurons, exfoliated deciduous stem cells-differentiated dopaminergic neurons [108], retinal ganglion cells [105], neuroblastoma [109], cultured cardiomyocytes [110], and placenta trophoblasts [111].…”

Section: Bdnf In Skeletal Musclementioning

confidence: 99%

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Is Brain-Derived Neurotrophic Factor a Metabolic Hormone in Peripheral Tissues?

Chan

2022

Biology

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Brain-derived neurotrophic factor (BDNF) is an important growth factor in the central nervous system. In addition to its well-known activities in promoting neuronal survival, neuron differentiation, and synaptic plasticity, neuronal BDNF also regulates energy homeostasis by modulating the hypothalamus’s hormonal signals. In the past decades, several peripheral tissues, including liver, skeletal muscle, and white adipose tissue, were demonstrated as the active sources of BDNF synthesis in response to different metabolic challenges. Nevertheless, the functions of BDNF in these tissues remain obscure. With the use of tissue-specific Bdnf knockout animals and the availability of non-peptidyl BDNF mimetic, increasing evidence has reported that peripheral tissues-derived BDNF might play a significant role in maintaining systemic metabolism, possibly through the regulation of mitochondrial dynamics in the various tissues. This article reviews the autocrine/paracrine/endocrine functions of BDNF in non-neuronal tissues and discusses the unresolved questions about BDNF’s function.

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“…Among them, PomE exerted strong effects on the activation of thermogenesis—lipolysis, β-oxidation, and uncoupling—and mitochondrial metabolism in in vitro cell models [ 8 ]. At the molecular level, PomE augmented the expression of UCP1 , UCP2 , BMP8B , CKMT , AMPK , and PRDM16 , which are key regulators of mitochondrial function and thermogenesis in differentiated human adipocytes [ 9 , 10 , 11 , 12 , 13 ], as well the expression of key myokines such as BDNF in differentiated myocytes, which has been described as a paracrine effector of browning [ 14 , 15 , 16 ]. Importantly, PomE enhanced the mitochondrial respiration capacity and the uncoupling and proton leakage in adipocytes and myocytes in vitro.…”

Section: Introductionmentioning

confidence: 99%

Pomegranate Extract Augments Energy Expenditure Counteracting the Metabolic Stress Associated with High-Fat-Diet-Induced Obesity

Reguero

Cedrón

Sierra-Ramírez

et al. 2022

IJMS

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Obesity is associated to a low grade of chronic inflammation leading to metabolic stress, insulin resistance, metabolic syndrome, dislipidemia, cardiovascular disease, and even cancer. A Mediterranean diet has been shown to reduce systemic inflammatory factors, insulin resistance, and metabolic syndrome. In this scenario, precision nutrition may provide complementary approaches to target the metabolic alterations associated to “unhealthy obesity”. In a previous work, we described a pomegranate extract (PomE) rich in punicalagines to augment markers of browning and thermogenesis in human differentiated adipocytes and to augment the oxidative respiratory capacity in human differentiated myocytes. Herein, we have conducted a preclinical study of high-fat-diet (HFD)-induced obesity where PomE augments the systemic energy expenditure (EE) contributing to a reduction in the low grade of chronic inflammation and insulin resistance associated to obesity. At the molecular level, PomE promotes browning and thermogenesis in adipose tissue, reducing inflammatory markers and augmenting the reductive potential to control the oxidative stress associated to the HFD. PomE merits further investigation as a complementary approach to alleviate obesity, reducing the low grade of chronic inflammation and metabolic stress.

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Brain-derived neurotrophic factor modulates mitochondrial dynamics and thermogenic phenotype on 3T3-L1 adipocytes

Cited by 13 publications

References 40 publications

Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle—Do Myokines Play a Role?

Mitochondria Homeostasis and Oxidant/Antioxidant Balance in Skeletal Muscle—Do Myokines Play a Role?

Is Brain-Derived Neurotrophic Factor a Metabolic Hormone in Peripheral Tissues?

Pomegranate Extract Augments Energy Expenditure Counteracting the Metabolic Stress Associated with High-Fat-Diet-Induced Obesity

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