Brown fat in obesity: Uncoupling protein-1 versus thermogenic activity

Madden, Christopher J.

doi:10.1080/23328940.2017.1317380

Cited by 5 publications

(5 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, anatomical differences in both brown and brown-like adipocytes were observed between humans and animals [2,10]. Another reason could be that obese animals displayed more UCP1 than lean animals, the opposite trend of humans [48], which indicates differences in UCP1 adaptations to exercise between animals and humans.…”

Section: Discussionmentioning

confidence: 99%

Human white-fat thermogenesis: Experimental and meta-analytic findings

et al. 2020

View full text Add to dashboard Cite

White adipose tissue (WAT) thermogenic activity may play a role in whole-body energy balance and two of its main regulators are thought to be environmental temperature (T env) and exercise. Low T env may increase uncoupling protein one (UCP1; the main biomarker of thermogenic activity) in WAT to regulate body temperature. On the other hand, exercise may stimulate UCP1 in WAT, which is thought to alter body weight regulation. However, our understanding of the roles (if any) of T env and exercise in WAT thermogenic activity remains incomplete. Our aim was to examine the impacts of low T env and exercise on WAT thermogenic activity, which may alter energy homeostasis and body weight regulation. We conducted a series of four experimental studies, supported by two systematic reviews and meta-analyses. We found increased UCP1 mRNA (p = 0.03; but not protein level) in human WAT biopsy samples collected during the cold part of the year, a finding supported by a systematic review and meta-analysis (PROSPERO review protocol: CRD42019120116). Additional clinical trials (NCT04037371; NCT04037410) using Positron Emission Tomography/Computed Tomography (PET/CT) revealed no impact of low T env on human WAT thermogenic activity (p > 0.05). Furthermore, we found no effects of exercise on UCP1 mRNA or protein levels (p > 0.05) in WAT biopsy samples from a human randomized controlled trial (Clinical trial: NCT04039685), a finding supported by systematic review and metaanalytic data (PROSPERO review protocol: CRD42019120213). Taken together, the present experimental and meta-analytic findings of UCP1 and SUV max , demonstrate that cold and exercise may play insignificant roles in human WAT thermogenic activity.

show abstract

Section: Discussionmentioning

confidence: 99%

Human white-fat thermogenesis: Experimental and meta-analytic findings

et al. 2020

View full text Add to dashboard Cite

show abstract

“… The role of endogenous opioids in thermoregulation might benefit from a discussion of the role of kappa opioid receptors in high fat diet induced impairment of BAT activation. (see Conceicao et al , eNeuro, 2021 12 (my paper)) and the parallels between animals maintained on a high fat diet and hibernation (see my paper, Madden, Temperature, 2017 13 ). The suggestion that hypothermia-inducing DMH neurons are cholinergic is insightful and interesting.…”

mentioning

confidence: 89%

Turn it off and on again: characteristics and control of torpor

2021

View full text Add to dashboard Cite

Torpor is a hypothermic, hypoactive, hypometabolic state entered into by a wide range of animals in response to environmental challenge. This review summarises the current understanding of torpor. We start by describing the characteristics of the wide-ranging physiological adaptations associated with torpor. Next follows a discussion of thermoregulation, control of food intake and energy expenditure, and the interactions of sleep and thermoregulation, with particular emphasis on how those processes pertain to torpor. We move on to take a critical view of the evidence for the systems that control torpor entry, including both the efferent circulating factors that signal the need for torpor, and the central processes that orchestrate it. Finally, we consider how the putative circuits responsible for torpor induction integrate with the established understanding of thermoregulation under non-torpid conditions and highlight important areas of uncertainty for future studies.

show abstract

“…Recent clinical and experimental studies have shed light on some molecular mechanisms linking excessive fatty acid oxidation and tumorkines to rapid mobilization of lipids from adipose tissue (Nieman et al, ; Tsoli et al, ). In another context, It has been shown that levels of BAT are markedly reduced in obese individuals (Madden, ). This, coupled with the idea that BAT contributes toward increased levels of energy expenditure, has led it to be a target for the treatment of obesity (Madden, ).…”

Section: Adipose Tissue Dysfunction In Cancer Cachexiamentioning

confidence: 99%

“…In another context, It has been shown that levels of BAT are markedly reduced in obese individuals (Madden, ). This, coupled with the idea that BAT contributes toward increased levels of energy expenditure, has led it to be a target for the treatment of obesity (Madden, ).…”

Section: Adipose Tissue Dysfunction In Cancer Cachexiamentioning

confidence: 99%

Adipose tissue dysfunction in cancer cachexia

Da’as

Rizeq

Nasrallah

2018

Journal Cellular Physiology

113

View full text Add to dashboard Cite

Cancer cachexia is a complex disorder that is driven by inflammation and metabolic imbalances, resulting in extreme weight loss. Adipose tissue, a main player in cancer cachexia, is an essential metabolic and secretory organ consisting of both white adipose tissue (WAT) and brown adipose tissue. Its secretory products, including adipokines and cytokines, affect a wide variety of central and peripheral organs, such as the skeletal muscle, brain, pancreas, and liver. Therefore, a combination of metabolic alterations, and systemic inflammation dysregulation of both anti-inflammatory and proinflammatory modulators contribute toward adipose tissue wasting in cancer cachexia. Growing evidence suggests that, during cancer cachexia, WAT undergoes a browning process, resulting in increased lipid mobilization and energy expenditure. In this review, we have summarized the characteristics of cancer cachexia and WAT browning. Furthermore, this review describes how adipose tissue becomes inflamed in cancer, shedding light on the combinatorial action of multiple secreted macromolecules, cytokines, hormones, and tumor mediators on adipose tissue dysfunction. We also highlight the inflammatory responses, energy utilization defects, and molecular mechanisms underlying the WAT dysfunction and browning in cancer cachexia. Further, the actual mechanisms behind the loss of adipose tissue are unknown, but have been attributed to increased adipocyte lipolysis, systemic inflammation, and apoptosis or reduced lipogenesis. The understanding of adipose tissue dysfunction in cancer cachexia will hopefully promote the development of new therapeutic approaches to prevent or treat this wasting syndrome.

show abstract

Brown fat in obesity: Uncoupling protein-1 versus thermogenic activity

Cited by 5 publications

References 6 publications

Human white-fat thermogenesis: Experimental and meta-analytic findings

Human white-fat thermogenesis: Experimental and meta-analytic findings

Turn it off and on again: characteristics and control of torpor

Adipose tissue dysfunction in cancer cachexia

Contact Info

Product

Resources

About