CD36 is important for adipocyte recruitment and affects lipolysis

Vroegrijk, Irene O.C.M.; Klinken, Jan B. van; Diepen, Janna A. van; Berg, Sjoerd A.A. van den; Febbraio, Maria; Steinbusch, Laura K. M.; Glatz, Jan F. C.; Havekes, Louis M.; Voshol, Peter J.; Rensen, Patrick C.N.; Dijk, Ko Willems van; Harmelen, Vanessa van

doi:10.1002/oby.20354

Cited by 59 publications

(50 citation statements)

References 33 publications

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“…Isolated adipocytes from CD36 KO mice have impaired NEFA uptake (Coburn et al, 2000). Furthermore, CD36-deficient mice do not develop diet-induced obesity, suggesting that adipocyte hypertrophy is impaired in these mice (Hajri et al, 2007;Koonen et al, 2010;Vroegrijk et al, 2013). We speculate that increased circulating lipid causes adipocyte hypertrophy and adipose growth, but there is currently limited evidence to show clearly that circulating lipid levels induce a hypertrophic morphology, as defined by Arner et al (2010).…”

Section: Availability Of Lipid As a Rate-limiting Step For Adipocyte mentioning

confidence: 79%

Adipose morphology and metabolic disease

Tandon

Wafer

Minchin

2018

Journal of Experimental Biology

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Adipose morphology is defined as the number and size distribution of adipocytes (fat cells) within adipose tissue. Adipose tissue with fewer but larger adipocytes is said to have a 'hypertrophic' morphology, whereas adipose with many adipocytes of a smaller size is said to have a 'hyperplastic' morphology. Hypertrophic adipose morphology is positively associated with insulin resistance, diabetes and cardiovascular disease. By contrast, hyperplastic morphology is associated with improved metabolic parameters. These phenotypic associations suggest that adipose morphology influences risk of cardiometabolic disease. Intriguingly, monozygotic twin studies have determined that adipose morphology is in part determined genetically. Therefore, identifying the genetic regulation of adipose morphology may help us to predict, prevent and ameliorate insulin resistance and associated metabolic diseases. Here, we review the current literature regarding adipose morphology in relation to: (1) metabolic and medical implications; (2) the methods used to assess adipose morphology; and (3) transcriptional differences between morphologies. We further highlight three mechanisms that have been hypothesized to promote adipocyte hypertrophy and thus to regulate adipose morphology.

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Section: Availability Of Lipid As a Rate-limiting Step For Adipocyte mentioning

confidence: 79%

Adipose morphology and metabolic disease

Tandon

Wafer

Minchin

2018

Journal of Experimental Biology

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“…(79) A study of CD36 knockout mice revealed reduced bone quantity, suggesting that CD36 is important for skeletal health. (79) A study of CD36 knockout mice revealed reduced bone quantity, suggesting that CD36 is important for skeletal health.…”

Section: Discussionmentioning

confidence: 99%

Exercise Degrades Bone in Caloric Restriction, Despite Suppression of Marrow Adipose Tissue (MAT)

McGrath

Sankaran

Misaghian‐Xanthos

et al. 2019

Journal of Bone and Mineral Research

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Marrow adipose tissue (MAT) and its relevance to skeletal health during caloric restriction (CR) is unknown: It remains unclear whether exercise, which is anabolic to bone in a calorie‐replete state, alters bone or MAT in CR. We hypothesized that response of bone and MAT to exercise in CR differs from the calorie‐replete state. Ten‐week‐old female B6 mice fed a regular diet (RD) or 30% CR diet were allocated to sedentary (RD, CR, n = 10/group) or running exercise (RD‐E, CR‐E, n = 7/group). After 6 weeks, CR mice weighed 20% less than RD, p < 0.001; exercise did not affect weight. Femoral bone volume (BV) via 3D MRI was 20% lower in CR versus RD (p < 0.0001). CR was associated with decreased bone by μCT: Tb.Th was 16% less in CR versus RD, p < 0.003, Ct.Th was 5% less, p < 0.07. In CR‐E, Tb.Th was 40% less than RD‐E, p < 0.0001. Exercise increased Tb.Th in RD (+23% RD‐E versus RD, p < 0.003) but failed to do so in CR. Cortical porosity increased after exercise in CR (+28%, p = 0.04), suggesting exercise during CR is deleterious to bone. In terms of bone fat, metaphyseal MAT/ BV rose 159% in CR versus RD, p = 0.003 via 3D MRI. Exercise decreased MAT/BV by 52% in RD, p < 0.05, and also suppressed MAT in CR (−121%, p = 0.047). Histomorphometric analysis of adipocyte area correlated with MAT by MRI (R2 = 0.6233, p < 0.0001). With respect to bone, TRAP and Sost mRNA were reduced in CR. Intriguingly, the repressed Sost in CR rose with exercise and may underlie the failure of CR‐bone quantity to increase in response to exercise. Notably, CD36, a marker of fatty acid uptake, rose 4088% in CR (p < 0.01 versus RD), suggesting that basal increases in MAT during calorie restriction serve to supply local energy needs and are depleted during exercise with a negative impact on bone. © 2019 The Authors. Journal of Bone and Mineral Research published by American Society for Bone and Mineral Research.

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“…Tissues were processed for adipocyte size determination as previously described [18]. Adipocyte number per fat pad was calculated from the fat pad mass and adipocyte size.…”

Section: Methodsmentioning

confidence: 99%

The limited storage capacity of gonadal adipose tissue directs the development of metabolic disorders in male C57Bl/6J mice

et al. 2015

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Aims/hypothesisWhite adipose tissue (WAT) consists of various depots with different adipocyte functionality and immune cell composition. Knowledge of WAT-depot-specific differences in expandability and immune cell influx during the development of obesity is limited, therefore we aimed to characterise different WAT depots during the development of obesity in mice.MethodsGonadal WAT (gWAT), subcutaneous WAT (sWAT) and mesenteric WAT (mWAT) were isolated from male C57Bl/6J mice with different body weights (approximately 25–60 g) and analysed. Linear and non-linear regression models were used to describe the extent of WAT depot expandability and immune cell composition as a function of body weight.ResultsWhereas mouse sWAT and mWAT continued to expand with body weight, gWAT expanded mainly during the initial phase of body weight gain. The expansion diminished after the mice reached a body weight of around 40 g. From this point on, gWAT crown-like structure formation, liver steatosis and insulin resistance occurred. Mouse WAT depots showed major differences in immune cell composition: gWAT consisted mainly of macrophages, whereas sWAT and mWAT primarily contained lymphocytes.Conclusions/interpretationMarked inter-depot differences exist in WAT immune cell composition and expandability. The limited storage capacity of gWAT seems to direct the development of metabolic disorders in male C57Bl/6J mice.Electronic supplementary materialThe online version of this article (doi:10.1007/s00125-015-3594-8) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

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CD36 is important for adipocyte recruitment and affects lipolysis

Cited by 59 publications

References 33 publications

Adipose morphology and metabolic disease

Adipose morphology and metabolic disease

Exercise Degrades Bone in Caloric Restriction, Despite Suppression of Marrow Adipose Tissue (MAT)

The limited storage capacity of gonadal adipose tissue directs the development of metabolic disorders in male C57Bl/6J mice

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