Adipose cell hypertrophy precedes the appearance of small adipocytes by 3 days in C57BL/6 mouse upon changing to a high fat diet

Abstract

(2016) Adipose cell hypertrophy precedes the appearance of small adipocytes by 3 days in C57BL/6 mouse upon changing to a high fat diet, Adipocyte, 5:1, 81-87, DOI: 10.1080/21623945.2015 ABSTRACTAdipose tissue is the energy buffer in mammals. The cellularity of adipose tissue has a major role in determining the response of adipose tissue to insulin action. A reduction in the ability of adipose tissue to store ingested caloric excess can lead to dyslipidemia and lipotoxicity, impacting insulin action systemically. The dynamic response of adipose tissue to changes in diet is therefore a crucial aspect of metabolism, and has attracted attention in the context of the ongoing worldwide increase in overweight and obesity and resulting metabolic syndrome dysfunctions. We investigated in a mouse model if there is a specific delay between an increase in caloric intake and the recruitment of new adipocytes, and if there are other changes in adipose tissue dynamics concomitant with such a diet change. By developing a dynamic mathematical model, we found that there is a delay of 3 days between the start of a high fat diet and the recruitment of new adipocytes, and that the rate of fat mass increase modulates lipid turnover and adipose cell hypertrophy.

Thylakoids reduce body fat and fat cell size by binding to dietary fat making it less available for absorption in high-fat fed mice

“…5b). Overall, the cell size distribution of thylHFD fed mice was comparable with the distribution curve from chow-fed mice, reported previously [12] (Fig. 5a).…”

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Fig. 5 a - b Adipocyte size distribution a in large versus small cell fraction (defined as above and below the nadir point, marked with arrow), dotted line represents previous reported cell size distribution of chow-fed mice (chow control group) [12], here inserted for comparison. The mean cell size of the cells in the large fraction b from mice fed HFD vs ThylHFD for two weeks.

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“…This could be fecal fat excretion and/or a recruitment of new adipocytes that have a more active metabolism. When storing energy, adipocytes initially grow in size, followed by differentiation and recruitment of new adipocytes [11, 12]. Special genes have been identified, the PPAR genes, which when activated increase the number of adipocytes so as to direct the energy to small adipocytes, which are less inflammatory [13].…”

Proliferation of nutrition sensing preadipocytes upon short term HFD feeding

“…2,3 Long-and short-term overnutrition has been shown to directly influence adipose tissue and to cause hypertrophy, inflammation, insulin resistance, and changes in plasma parameters in mice and humans. 2,[4][5][6][7][8][9] Conversely, removal of HFD was shown to reverse most of these changes. 2,10,11 For some time it was believed, that the total number of fat cells is set during adolescence and a change of fat mass in adults is exclusively caused by hypertrophy.…”

EHD2 regulates adipocyte function and is enriched at cell surface–associated lipid droplets in primary human adipocytes

“…Impaired energy storage capacity in adipocytes is associated with increased levels of circulating FFA and with ectopic lipid accumulation in liver and muscle, which is a major risk factor for developing insulin resistance and type 2 diabetes (Schinner et al , 2005). We and others have examined the dynamics of adipose tissue expansion (McLaughlin et al , 2007; Li et al , 2016; Hansson et al , 2018), which involves increased adipocyte size (hypertrophy) as well as increased cell number (hyperplasia). The latter occurs through differentiation of preadipocytes (adipogenesis) (Salans et al , 1968), a process tightly regulated by various transcription factors, including peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins alpha and beta (C/EBPα and C/EBPβ).…”