Markers of de novo lipogenesis in adipose tissue: associations with small adipocytes and insulin sensitivity in humans

Abstract

Aims/hypothesis Previous studies have shown relationships between fatty acid ratios in adipose tissue triacylglycerol (TG), adipocyte size and measures of insulin sensitivity. We hypothesised that variations in adipose tissue de novo lipogenesis (DNL) in relation to adiposity might explain some of these observations. Methods In a cross-sectional study, subcutaneous abdominal adipose tissue biopsies from 59 people were examined in relation to fasting and post-glucose insulin sensitivity. Adipocyte size, TG fatty acid composition and mRNA expression of lipogenic genes were determined. Results We found strong positive relationships between adipose tissue TG content of the fatty acids myristic acid (14:0) and stearic acid (18:0) with insulin sensitivity (HOMA model) (p<0.01 for each), and inverse relationships with adipocyte size (p<0.01, p<0.05, respectively).

Adipose tissue fatty acids and insulin sensitivity in elderly men

“…However, if this were the case, one would expect a similar pattern for 15:0 and 17:0, also considered closely associated with dairy intake when measured in serum [29] or erythrocyte membranes [30]. For 15:0, this was not significant in our study, suggesting that other dietary sources of 14:0, or endogenous metabolism, may contribute to the association, as also recently suggested by Roberts et al [19]. The positive association between 18:0 and insulin sensitivity also accord with that study, in which adipose tissue 14:0 and 18:0 were positively associated with HOMA insulin sensitivity, whereas 16:0 was inversely correlated in a group of 59 healthy individuals.…”

“…The positive association between 18:0 and insulin sensitivity also accord with that study, in which adipose tissue 14:0 and 18:0 were positively associated with HOMA insulin sensitivity, whereas 16:0 was inversely correlated in a group of 59 healthy individuals. The positive association between 14:0 and 18:0 and insulin sensitivity was suggested to mainly reflect de novo lipogenesis (DNL), since no correlation was seen between SFA intake and adipose tissue content of these fatty acids [19]. In our larger population study, we did, however, observe significant but weak associations between dietary SFA intake and adipose tissue SFAs.…”

“…Whether carbohydrate intake may partly contribute to increased SFA proportions could also be considered, although there is little evidence to support this [19] and adipose tissue DNL seems to be minor in Western populations [31], including Sweden, consuming ∼45% of energy as carbohydrate in 1989 [26]. It was further suggested by Roberts et al that the relationship between SFAs and insulin sensitivity may be stronger in lean individuals, partly because of smaller adipocyte size and lipogenesis [19]. However, in our secondary analyses, stratified by BMI, we could not observe this in our elderly Swedish population.…”

“…As renewal of fatty acids in adipose tissue is slow, its composition reflects dietary intake over 0.5-2 years [13,15,16]. Another limitation of previous studies is the use of indirect measurements of insulin sensitivity, such as fasting insulin concentrations [17] or HOMA indices [18,19].…”

Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation

“…Moreover, zinc has insulin-like effects in adipocytes, stimulating lipogenesis and increasing fatty acid accumulation (57,58). Consistent with effects of adipocyte zinc accumulation, we observed adipocyte hypertrophy in ZnT2-null mammary glands, which could indicate increased lipogenesis (59). Therefore, the loss of ZnT2 in adipocytes may mirror insulinlike effects on lipogenesis that stunt ductal growth (60) or may affect the synthesis or release of paracrine factors, such as adiponectin and collagen VI (61) from adipocytes that initiate epithelial/mesenchymal interaction and facilitate ductal expansion (55).…”