Exercise does not induce browning of WAT at thermoneutrality and induces an oxidative, myogenic signature in BAT

Aldiss, Peter; Lewis, Jo; Lupini, Irene; Boocock, David J.; Miles, Amanda K.; Ebling, F. J.; Budge, Helen; Symonds, Michael

doi:10.1101/649061

Cited by 9 publications

(13 citation statements)

References 52 publications

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“…Elucidating protein-protein interactions (PPI) is an important step in understanding both communication between proteins following an intervention and the identification of novel signalling pathways. We have previously shown that ribosomal proteins are important hub proteins in PPI networks following exercise training and, in the present study, show that these also respond to YM-178 [9]. Furthermore, these interact with multiple other mitochondrial ribosomal proteins and proteins governing energy metabolism such as mTOR and leptin.…”

Section: Discussionsupporting

confidence: 64%

“…Next, we analysed a panel of primary thermogenic genes in BAT and PVAT as we have previously shown these two anatomically and developmentally distinct BAT depots exhibit a divergent response to both a brief period of nutrient excess and exercise training [9, 11]. Despite an increase in BAT mass with cold, there was no reduction in thermogenic genes (i.e.…”

Section: Resultsmentioning

confidence: 99%

“…standard housing temperatures (20°C)), which constitutes a drop of c. 8°C and chronic β3-AR agonism in animals raised from weaning at thermoneutrality. Using this model, in which animals are not ‘cold-stressed’ and BAT is chronically inactive, we have demonstrated UCP1 mRNA is absent in subcutaneous IWAT (the classical ‘beige’ depot) and not induced with exercise training, a common response at standard housing temperatures [9]. We hypothesised that exposure to a mild cold stimulus in animals raised at thermoneutrality would have modest effects on systemic metabolism but not weight per se.…”

Section: Introductionmentioning

confidence: 99%

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Cold exposure drives weight gain and adiposity following chronic suppression of brown adipose tissue

Aldiss

Lewis

Lupini

et al. 2019

Preprint

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Background and aim:Rodents are commonly housed below thermoneutrality and this exposure to 'cold' (i.e. 20°C) activates thermogenic brown (BAT) and beiging of white adipose tissue. Here, we examined whether a standard housing temperature (i.e. 20°C, a reduction in temperature of ~8°C) or YM-178, a highly-selective β 3-adrenoreceptor agonist, in obese animals raised at thermoneutrality, would impact differently on classical BAT or subcutaneous inguinal (IWAT) beige depots. Methods: Eighteen weanling Sprague-Dawley rats were housed at thermoneutrality (28°C) and fed a high-fat diet. At 12 weeks, 6 animals were randomised to either standard housing temperature (20°C, n=6) or to β 3-AR agonist administration (28°C+β3, 0.75mg/kg/d, n=6) for 4 weeks. Metabolic assessment was undertaken during the final 48h, followed by interscapular, perivascular BAT and IWAT sampling for the analysis of thermogenic genes and the proteome. Results: Exposure to 20°C increased weight gain, BAT and IWAT mass. Proteomic analysis of BAT revealed novel pathways associated with cold-induced weight gain (i.e. histone deacetylation, glycosaminoglycan degradation and glycosphingolipid biosynthesis) whilst β 3adrenoreceptor agonism impacted on proteins involved in skeletal muscle contraction and cell differentiation. IWAT of cold-exposed animals exhibited an enrichment of proteins involved NAD+ binding, plus retinol and tyrosine metabolic pathways whilst β 3-AR agonism downregulated ribosomal and upregulated acute phase response proteins. Conclusion: Following diet-induced obesity at thermoneutrality, exposure to 20°C promotes subcutaneous fat deposition in order to reduce heat loss and defend body temperature. In contrast, chronic administration of β 3-AR agonist has minimal metabolic-related effects on adipose tissue.

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Section: Discussionsupporting

confidence: 64%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cold exposure drives weight gain and adiposity following chronic suppression of brown adipose tissue

Aldiss

Lewis

Lupini

et al. 2019

Preprint

Self Cite

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“…We assessed the metabolic responses of skeletal muscle and liver by determining the expression of key genes involved in energy metabolism and metabolic serum parameters including acylcarnitines, ketone bodies, and glycemia. We also assessed the effect of the above protocol on (a) serum levels of thyroid hormone, the action of which is known to partially mimic the response to exercise (Aldiss et al, 2019) (Muscedola s.r.l., Milan, Italy). The animals were acclimated to the 28°C housing temperature for 3 weeks, being familiarized with the treadmill (Panlab, Harvard Apparatus).…”

Section: Introductionmentioning

confidence: 99%

Exercise with food withdrawal at thermoneutrality impacts fuel use, the microbiome, AMPK phosphorylation, muscle fibers, and thyroid hormone levels in rats

et al. 2020

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Exercise under fasting conditions induces a switch to lipid metabolism, eliciting beneficial metabolic effects. Knowledge of signaling responses underlying metabolic adjustments in such conditions may help to identify therapeutic strategies. Therefore, we studied the effect of mild exercise on rats submitted to food withdrawal at thermoneutrality (28°C) for 3 days. Animals were housed at thermoneutrality rather than the standard housing temperature (22°C) to avoid beta‐adrenergic signaling responses that themselves affect metabolism and well‐being. Quantitative analysis of multi‐organ mRNA levels, myofibers, and serum metabolites shows that this protocol (a) boosts fat oxidation in muscle and liver, (b) reduces lipogenesis and increases gluconeogenesis in liver, (c) increases serum acylcarnitines (especially C4OH) and ketone bodies and the use of the latter as fuel in muscle, (d) increases Type I myofibers, and (e) is associated with an increased thyroid hormone uptake and metabolism in muscle. In addition, stool microbiome DNA analysis revealed that food withdrawal dramatically alters the presence of bacterial genera associated with ketone metabolism. Taken together, this protocol induces a drastic switch toward increased lipid and ketone metabolism compared to exercise or food withdrawal alone, which may prove beneficial and may involve local thyroid hormones, which may be regarded as exercise mimetics.

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“…During obesity and aging, the gradual shift into WAT-like characteristics of PVAT is associated with the alteration of secretome profile, which may lead to vascular dysfunction, arterial remodeling and increase in blood pressure [ 62 , 63 ]. Apart from cold exposure, exercise training has been shown to induce a BAT-like shift and thermogenic response, which is associated with enhanced eNOS expression and reduced oxidative stress in PVAT [ 64 ].…”

Section: Role Of Adipose Tissue In Metabolic and Cardiovascular Hementioning

confidence: 99%

Circadian Rhythm in Adipose Tissue: Novel Antioxidant Target for Metabolic and Cardiovascular Diseases

Man¹,

Xia²,

Li³

2020

Antioxidants

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Obesity is a major risk factor for most metabolic and cardiovascular disorders. Adipose tissue is an important endocrine organ that modulates metabolic and cardiovascular health by secreting signaling molecules. Oxidative stress is a common mechanism associated with metabolic and cardiovascular complications including obesity, type 2 diabetes, and hypertension. Oxidative stress can cause adipose tissue dysfunction. Accumulating data from both humans and experimental animal models suggest that adipose tissue function and oxidative stress have an innate connection with the intrinsic biological clock. Circadian clock orchestrates biological processes in adjusting to daily environmental changes according to internal or external cues. Recent studies have identified the genes and molecular pathways exhibiting circadian expression patterns in adipose tissue. Disruption of the circadian rhythmicity has been suggested to augment oxidative stress and aberrate adipose tissue function and metabolism. Therefore, circadian machinery in the adipose tissue may be a novel therapeutic target for the prevention and treatment of metabolic and cardiovascular diseases. In this review, we summarize recent findings on circadian rhythm and oxidative stress in adipose tissue, dissect the key components that play a role in regulating the clock rhythm, oxidative stress and adipose tissue function, and discuss the potential use of antioxidant treatment on metabolic and cardiovascular diseases by targeting the adipose clock.

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Exercise does not induce browning of WAT at thermoneutrality and induces an oxidative, myogenic signature in BAT

Cited by 9 publications

References 52 publications

Cold exposure drives weight gain and adiposity following chronic suppression of brown adipose tissue

Cold exposure drives weight gain and adiposity following chronic suppression of brown adipose tissue

Exercise with food withdrawal at thermoneutrality impacts fuel use, the microbiome, AMPK phosphorylation, muscle fibers, and thyroid hormone levels in rats

Circadian Rhythm in Adipose Tissue: Novel Antioxidant Target for Metabolic and Cardiovascular Diseases

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