scholarly journals A distribution-centered approach for analyzing human adipocyte size estimates and their association with obesity-related traits and mitochondrial function

Author(s):  
Julius Honecker ◽  
Dominik Weidlich ◽  
Simone Heisz ◽  
Cecilia M. Lindgren ◽  
Dimitrios C. Karampinos ◽  
...  

Abstract Objective Cell diameter, area, and volume are established quantitative measures of adipocyte size. However, these different adipocyte sizing parameters have not yet been directly compared regarding their distributions. Therefore, the study aimed to investigate how these adipocyte size measures differ in their distribution and assessed their correlation with anthropometry and laboratory chemistry. In addition, we were interested to investigate the relationship between fat cell size and adipocyte mitochondrial respiratory chain capacity. Methods Subcutaneous and visceral histology-based adipocyte size estimates from 188 individuals were analyzed by applying a panel of parameters to describe the underlying cell population. Histology-based adipocyte diameter distributions were compared with adipocyte diameter distributions from collagenase digestion. Associations of mean adipocyte size with body mass index (BMI), glucose, HbA1C, blood lipids as well as mature adipocyte mitochondrial respiration were investigated. Results All adipocyte area estimates derived from adipose tissue histology were not normally distributed, but rather characterized by positive skewness. The shape of the size distribution depends on the adipocyte sizing parameter and on the method used to determine adipocyte size. Despite different distribution shapes histology-derived adipocyte area, diameter, volume, and surface area consistently showed positive correlations with BMI. Furthermore, associations between adipocyte sizing parameters and glucose, HbA1C, or HDL specifically in the visceral adipose depot were revealed. Increasing subcutaneous adipocyte diameter was negatively correlated with adipocyte mitochondrial respiration. Conclusions Despite different underlying size distributions, the correlation with obesity-related traits was consistent across adipocyte sizing parameters. Decreased mitochondrial respiratory capacity with increasing subcutaneous adipocyte diameter could display a novel link between adipocyte hypertrophy and adipose tissue function.

Zygote ◽  
1999 ◽  
Vol 8 (S1) ◽  
pp. S3-S4
Author(s):  
Ikuo Yasumasu

It is well known that sea urchin eggs, which exhibit quite a low rate of respiration before fertilisation, undergo a sudden increase in the rate of respiration followed by its gradual decrease in about a 15 min period after fertilisation (Ohnishi & Sugiyama, 1963; Epel, 1969), in which the respiration is mediated mainly by Ca2+-activated non-mitochondrial respiratory systems (Foerder et al., 1978; Perry & Epel, 1985a,b). During this short period the rate of mitochondrial respiration gradually increases (Yasumasu et al., 1988) and stabilises at a higher rate than before fertilisation (Warburg, 1908, 1910; Whitaker, 1933; Yasumasu & Nakano, 1963), when the respiration due to non-mitochondrial respiratory systems is turned off. The rate of mitochondrial respiration, once enhanced upon fertilisation, increases further in the period between hatching and the gastrula stage, without any changes in the number of mitochondria or the capacity of electron transport in the mitochondrial respiratory chain (Fujiwara & Yasumasu, 1997; Fujiwara et al., 2000). It is likely that the respiratory rate is reduced by regulation of electron transport in the mitochondrial respiratory chain and increases due to the release of electron transport from the regulation upon fertilisation and after hatching.A marked increase in the respiratory rate after hatching is accompanied by an evident decrease in the ATP level without any change in the levels of ADP and AMP (Mita & Yasumasu, 1984). In isolated mitochondria, the rate of respiration, estimated in the presence of ADP at the same concentration as in embryos, is reduced by a high concentration of ATP as found in embryos before hatching but is not affected at a concentration as low as in gastrulae (Fujiwara & Yasumasu, 1997; Fujiwara et al., 2000) ATP at a high concentration probably blocks ATP release from mitochondria and consequently inhibits ADP uptake coupled to ATP release in the ATP/ADP translocation reaction in the mitochondrial membrane, causing a shortage of intra-mitochondrial ADP.


2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Xuelian Zhang ◽  
Bin Zhang ◽  
Chenyang Zhang ◽  
Guibo Sun ◽  
Xiaobo Sun

AbstractTribbles homolog 1 (TRIB1) belongs to the Tribbles family of pseudokinases, which plays a key role in tumorigenesis and inflammation. Although genome-wide analysis shows that TRIB1 expression is highly correlated with blood lipid levels, the relationship between TRIB1 and adipose tissue metabolism remains unclear. Accordingly, the aim of the present study was to explore the role of TRIB1 on mitochondrial function in the brown adipose tissue (BAT). Trib1-knockout mice were established using clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technology. The metabolic function of the BAT was induced by a β3-adrenoceptor agonist and the energy metabolism function of mitochondria in the BAT of mice was evaluated. Trib1-knockout mice exhibited obesity and impaired BAT thermogenesis. In particular, Trib1 knockout reduced the ability of the BAT to maintain body temperature, inhibited β3-adrenoceptor agonist-induced thermogenesis, and accelerated lipid accumulation in the liver and adipose tissues. In addition, Trib1 knockout reduced mitochondrial respiratory chain complex III activity, produced an imbalance between mitochondrial fusion and fission, caused mitochondrial structural damage and dysfunction, and affected heat production and lipid metabolism in the BAT. Conversely, overexpression of Trib1 in 3T3-L1 adipocytes increased the number of mitochondria and improved respiratory function. These findings support the role of Trib1 in regulating the mitochondrial respiratory chain and mitochondrial dynamics by affecting mitochondrial function and thermogenesis in the BAT.


1984 ◽  
Vol 62 (12) ◽  
pp. 1448-1452 ◽  
Author(s):  
Roland Savard ◽  
Yves Deshaies ◽  
Jean-Pierre Després ◽  
Martine Marcotte ◽  
Ludwik Bukowiecki ◽  
...  

Lipogenesis from glucose and lipoprotein lipase activity were investigated in humans. The reliability of measurements was quantified and correlations with fat cell weight were assessed. Twenty-four subjects (7 women, 17 men) were studied twice within a 2-week period, along with 17 additional male subjects who were studied once and used only in the correlation analyses. All subjects were not regularly involved in an exercise-training program and were between 18 and 30 years of age. Following an overnight fast, adipose tissue specimens were obtained by suprailiac biopsy and fat cells were collagenase isolated. Mean fat cell weight was obtained from 400 to 500 cell diameter determinations per subject. Basal and insulin-stimulated fat cell lipogenesis from glucose were determined using D-[U-14C]glucose and were reported in nanomoles of glucose per hour per 106 cells. Adipose tissue heparin-releasable lipoprotein lipase activity was also determined and expressed in micromoles of free fatty acids per hour per gram of tissue and per 106 cells. Fat cell weight, basal and insulin-stimulated lipogenesis and lipoprotein lipase activity per gram showed high reliability of measurement, interclass and intraclass coefficients being 0.83 and over. Lipoprotein lipase activity per 106 cells showed a somewhat lower degree of reliability, interclass and intraclass coefficients being, respectively, 0.69 and 0.81. On the other hand, fat cell weight was positively correlated with lipoprotein lipase activity (r = 0.80), while no significant correlation was observed between basal lipogenesis and fat cell weight. Moreover, basal lipogenesis presented no significant correlation with lipoprotein lipase activity. These results suggest that, under standardized conditions, and from a single tissue sample, human adipose tissue lipoprotein lipase activity and fat cell lipogenesis can be measured with a satisfactory level of reliability. They also suggest that lipoprotein lipase activity is highly related with adipocyte lipid content.


1982 ◽  
Vol 35 (2) ◽  
pp. 185-192 ◽  
Author(s):  
R. G. Campbell ◽  
A. C. Dunkin

ABSTRACTForty-two piglets were used to study the effects of heavy and light birth weight, and of four levels of feeding, ranging from 37 to 91 g dry matter per kg M0 75 per day, on growth between 5 days of age and 6·5kg live weight, and on body composition, and the cellularity of muscle and subcutaneous adipose tissue, at the latter weight. The effects of birth weight and level of feeding to 6·5 kg on performance between 6·5 and 11 -5 kg, and on body composition at 11·5 kg, were also investigated.Light birth weight piglets grew more slowly to 6·5 kg than those of heavy birth weight (P < 0·05). However, birth weight had no effect on food conversion efficiency or on body composition.Each increment in feeding level resulted in increases in growth rate (P < 0·01), body fat content (P < 0·01) and average fat-cell diameter (P < 0·01) at 6·5 kg, but in decreases in body protein and water (P < 0·01).The weight of the m. semitendinosus at 6·5 kg was unaffected by either birth weight or level of feeding. However, the deoxyribonucleic acid content of the muscle at both 6·5 and 11·5 kg was less in light birth weight piglets fed at the lowest level prior to 6·5 kg (P < 0·05). These piglets also exhibited poorer growth performance subsequent to 6·5 kg than their heavier birth weight counterparts.Nevertheless, piglets of both light and heavy birth weight, fed at the lowest level to 6·5 kg, grew faster and more effficiently between 6·5 and 11·5kg (P < 0·05), and were leaner at 11·5kg than those previously fed at the highest level (P < 0·01). Average fat-cell diameter at 11·5kg was also less in pigs fed at the lowest level prior to 6·5kg (P < 0·01). Total deoxyribonucleic acid in subcutaneous adipose tissue at 11·5kg was unaffected by either birth weight or level of feeding prior to 6·5 kg.


1986 ◽  
Vol 250 (4) ◽  
pp. E480-E485 ◽  
Author(s):  
E. T. Poehlman ◽  
J. P. Despres ◽  
M. Marcotte ◽  
A. Tremblay ◽  
G. Theriault ◽  
...  

The present study investigated the interaction of genotype and short-term overfeeding on adipose tissue metabolism of six pairs of male monozygotic twins. The sedentary nonobese twins were submitted to a 22-day overfeeding period in which their normal daily intake was supplemented by an additional 1,000 kcal/day. A fat tissue biopsy was performed in the suprailiac region before and after overfeeding to determine fat cell diameter and basal and maximal stimulated epinephrine, norepinephrine, and isoproterenol lipolysis from collagenase-isolated fat cells. Fat cell basal and maximal insulin-stimulated glucose conversion into triglycerides (basal and stimulated lipogenesis) were measured using [14C]glucose. Adipose tissue heparin-releasable lipoprotein lipase activity (LPL) was also determined. A repeated measures analysis of variance revealed overfeeding induced significant elevations in basal lipogenesis (P less than 0.05) and fat cell diameter (P less than 0.05). No significant group changes were noted in basal, epinephrine-, norepinephrine-, and isoproterenol-stimulated lipolysis, insulin-stimulated lipogenesis, and LPL activity due to large individual variation in the response to overfeeding. However, significant intrapair resemblance was noted in the changes of the aforementioned variables, suggesting a coherent within-twin pair response, despite large between-pair variation in response. Less within-pair similarity was noted in changes in basal lipogenesis and fat cell diameter. The results of the present study suggest that overfeeding induced a large range of adipose tissue metabolic responses and that the genotype plays a role in determining the sensitivity of adipose tissue adaptation to caloric affluence.


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