The Role and Regulatory Mechanism of Brown Adipose Tissue Activation in Diet-Induced Thermogenesis in Health and Diseases

Chan, Pei-Chi; Hsieh, Po‐Shiuan

doi:10.3390/ijms23169448

Cited by 8 publications

(4 citation statements)

References 181 publications

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“…To demonstrate the existence of diet-induced thermogenesis, it is, however, not sufficient to demonstrate a higher rate of thermogenesis in animals that overeat. This is because the total thermogenic response to eating—that we can call ‘diet-induced thermogenesis’—includes what is referred to as ‘obligatory’ diet-induced thermogenesis [9]. This is the extra heat inevitably produced by the organism in the processes of digesting the food and transferring the energy into lipids, etc.…”

Section: Does Diet-induced Thermogenesis Exist?mentioning

confidence: 99%

Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men

Nedergaard,

von Essen,

Cannon

2023

Phil. Trans. R. Soc. B

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The issue under discussion here is whether a decrease in the degree of UCP1 activity (and brown adipose tissue activity in general) could be a cause of obesity in humans. This possibility principally requires the existence of the phenomenon of diet-induced thermogenesis. Obesity could be a consequence of a reduced functionality of diet-induced thermogenesis. Experiments in mice indicate that diet-induced thermogenesis exists and is dependent on the presence of UCP1 and thus of brown adipose tissue activity. Accordingly, many (but not all) experiments indicate that in the absence of UCP1, mice become obese. Whether similar mechanisms exist in humans is still unknown. A series of studies have indicated a correlation between obesity and low brown adipose tissue activity, but it may be so that the obesity itself may influence the estimates of brown adipose tissue activity (generally glucose uptake), partly explaining the relationship. Estimates of brown adipose tissue catabolizing activity would seem to indicate that it may possess a capacity sufficient to help maintain body weight, and obesity would thus be aggravated in its absence. This article is part of a discussion meeting issue ‘Causes of obesity: theories, conjectures and evidence (Part II)’.

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Section: Does Diet-induced Thermogenesis Exist?mentioning

confidence: 99%

Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men

Nedergaard,

von Essen,

Cannon

2023

Phil. Trans. R. Soc. B

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“…WAT also secretes several hormones and cytokines that regulate energy metabolism, immune function and inflammation [ 13 ]. On the other hand, the primary function of brown adipose tissue (BAT) is to generate heat through a process called thermogenesis [ 14 ]. This process occurs in specialized organelles called mitochondria, which contain a protein called uncoupling protein 1 (UCP1) that uncouples the electron transport chain from ATP synthesis, resulting in the production of heat instead of ATP [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic Analysis from Normal Glucose Tolerance to T2D of Obese Individuals Using Bioinformatic Tools

Errafii

Boujraf

Chikri

2023

IJMS

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Understanding the role of white adipose tissue (WAT) in the occurrence and progression of metabolic syndrome is of considerable interest; among the metabolic syndromes are obesity and type 2 diabetes (T2D). Insulin resistance is a key factor in the development of T2D. When the target cells become resistant to insulin, the pancreas responds by producing more insulin to try to lower blood glucose. Over time, this can lead to a state of hyperinsulinemia (high levels of insulin in the blood), which can further exacerbate insulin resistance and contribute to the development of T2D. In order to understand the difference between healthy and unhealthy obese individuals, we have used published transcriptomic profiling to compare differences between the WAT obtained from obese diabetics and subjects who are obese with normal glucose tolerance and insulin resistance. The identification of aberrantly expressed messenger RNA (mRNA) and the resulting molecular interactions and signaling networks is essential for a better understanding of the progression from normal glucose-tolerant obese individuals to obese diabetics. Computational analyses using Ingenuity Pathway Analysis (IPA) identified multiple activated signaling networks in obesity progression from insulin-resistant and normal glucose-tolerant (IR-NGT) individuals to those with T2D. The pathways affected are: Tumor Necrosis Factor (TNF), Extracellular signal-Regulated protein Kinase 1/2 ERK1/2, Interleukin 1 A (IL1A), Protein kinase C (Pkcs), Convertase C5, Vascular endothelial growth factor (Vegf), REL-associated protein (RELA), Interleukin1/1 B (IL1/1B), Triggering receptor expressed on myeloid cells (TREM1) and Nuclear factor KB1 (NFKB1) networks, while functional annotation highlighted Liver X Receptor (LXR) activation, phagosome formation, tumor microenvironment pathway, LPS/IL-1 mediated inhibition of RXR function, TREM1 signaling and IL-6 signaling. Together, by conducting a thorough bioinformatics study of protein-coding RNAs, prospective targets could be exploited to clarify the molecular pathways underlying the development of obesity-related type 2 diabetes.

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“…Brown adipose tissue (BAT) is a key organ for non‐shivering thermogenesis in mammals (Cannon & Nedergaard, 2004; Chan & Hsieh, 2022). Significant amounts of BAT are present in rodents throughout their lifespan and in newborn humans (Zhang et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Wnt10b knockdown promotes UCP1 expression in brown adipose tissue in mice

Jia,

Liu,

Liu

et al. 2023

Genes to Cells

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The effect of Wnt10b overexpression on adipose tissue development has been reported. However, the impact of Wnt10b knockdown on the function of brown adipose tissue (BAT) is yet largely unknown. Here, we used the CRISPR/Cas9 technique to generate Wnt10b‐knockdown (Wnt10b+/−) mice. We compared the development and thermogenic gene expression of interscapular BAT (iBAT) between Wnt10b+/− and Wnt10b+/+ mice under a chow diet, high‐fat diet (HFD), and cold exposure conditions. Moreover, the effect of Wnt10b knockdown on brown adipocyte function was tested via in vitro experiments. Results indicated that Wnt10b knockdown decreased the iBAT mass and the brown adipocyte size and enhanced thermogenic gene expression, including UCP1, under chow diet conditions. In addition, Wnt10b+/− mice appeared to be able to maintain their body temperature better than the control in a cold environment, accompanied by higher UCP1 protein expression. Intriguingly, even under HFD conditions, Wnt10b+/− mice still showed higher UCP1 expression, which was associated with an alleviated obesity phenotype. In vitro studies further evidenced the Wnt10b knockdown stimulation of UCP1 expression and suppression of the adipogenic program. This study indicates that Wnt10b knockdown enhances UCP1 expression and inhibits the adipogenic differentiation of brown adipocytes, providing a novel option for therapeutic interventions in adiposity.

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The Role and Regulatory Mechanism of Brown Adipose Tissue Activation in Diet-Induced Thermogenesis in Health and Diseases

Cited by 8 publications

References 181 publications

Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men

Brown adipose tissue: can it keep us slim? A discussion of the evidence for and against the existence of diet-induced thermogenesis in mice and men

Transcriptomic Analysis from Normal Glucose Tolerance to T2D of Obese Individuals Using Bioinformatic Tools

Wnt10b knockdown promotes UCP1 expression in brown adipose tissue in mice

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