Influence of Aging and Menstrual Status on Subcutaneous Fat Cell Lipolysis

2019 ◽  
Vol 105 (4) ◽  
pp. e955-e962 ◽  
Author(s):  
Mikael Rydén ◽  
Hui Gao ◽  
Peter Arner

Abstract Context Aging is accompanied by inhibited fat cell mobilization of fatty acids through lipolysis, which may contribute to decreased energy expenditure in elderly subjects. However, the influence of menstrual status is unknown. Objective To investigate the role of menstrual status on changes in lipolysis induced by aging. Design A longitudinal investigation with a mean 13-year interval. Setting Ambulatory study at a clinical academic unit. Participants Eighty-two continuously recruited women between 24 and 62 years of age and with body mass index 21 to 48 kg/m2 at first examination. Twenty-nine women continued to have normal menstruation, 42 developed irregular menstruation/menopause, and 11 had a perimenstrual/menopausal phenotype already at the first examination. Main outcome measure Lipolysis measured as glycerol release from isolated subcutaneous fat cells incubated in vitro. Results On average, body weight/body fat mass levels did not change over time. In all 3 groups, aging was associated with a similar decrease in spontaneous (basal) and catecholamine-stimulated lipolysis. The latter was due to decreased signal transduction through stimulatory beta adrenoceptors and increased alpha-2-adrenoceptor–mediated antilipolytic effects. Gene microarray data from adipose tissue at baseline and follow-up (n = 53) showed that a limited set of lipolysis-linked genes, including phosphodiesterase-3B, were altered over time, but this was independent of menstrual status. Fat cell size also decreased during aging, but this could not explain the decrease in lipolysis. Conclusions In women, the rate of fat cell lipolysis decreases during aging due to multiple alterations in spontaneous (basal) and catecholamine-induced lipolysis. This is independent of changes in menstrual status or fat cell size.

1989 ◽  
Vol 256 (6) ◽  
pp. R1286-R1292 ◽  
Author(s):  
J. Dark ◽  
J. S. Stern ◽  
I. Zucker

Ad libitum fed golden-mantled ground squirrels undergo marked annual fluctuations in body mass; during the first cycle, peak and trough masses were approximately 291 and approximately 192 g, respectively. Peak masses were significantly higher (9%) during the second than the first cycle, reflecting a 15% increase in fat-free dry mass and a 12% increase in lipid reserves. The reduction in body mass during the weight loss phase was almost entirely due to an 84% decrease in total lipid reserves and reflected a decrease in adipocyte size but not number. All measured fat depots decreased at similar rates, and there was no evidence of preferential utilization or sparing of individual depots. Fat cell size decreased progressively in each depot during the transition from peak to trough masses and did not vary among the several depots at any stage of annual cycle. Adipocyte number increased in parametrial and retroperitoneal depots but not in the subcutaneous fat between the first and second body mass peaks; fat cell size in these two depots decreased by 28 and 20%, respectively, from the first to the second peak in body mass. Reduced lipid filling of adipocytes at the second peak mass, concomitant with adipocyte hyperplasia, suggests that total lipid mass, not simply fat cell size, is regulated during the annual body mass cycle. Maturation of the subcutaneous fat depot before the initial entry into hibernation may be adaptive in providing insulation during dormancy.


Metabolism ◽  
1999 ◽  
Vol 48 (11) ◽  
pp. 1371-1377 ◽  
Author(s):  
Jolanda M.H. Elbers ◽  
Sigrid de Jong ◽  
Tom Teerlink ◽  
Henk Asscheman ◽  
Jacob C. Seidell ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Vaishali I. Parekh ◽  
Sita D. Modali ◽  
Shruti S. Desai ◽  
Sunita K. Agarwal

Lipoma in patients with the multiple endocrine neoplasia type 1 (MEN1) syndrome is a type of benign fat-cell tumor that has biallelic inactivation ofMEN1that encodes menin and could serve as a model to investigate normal and pathologic fat-cell (adipocyte) proliferation and function. The role of menin and its target genes in adipocytes is not known. We used in vitro differentiation to derive matched normal and menin-deficient adipocytes from wild type (WT) and menin-null (Men1-KO) mouse embryonic stem cells (mESCs), respectively, or 3T3-L1 cells without or with menin knockdown to investigate cell size, lipid content, and gene expression changes. Adipocytes derived from Men1-KO mESCs or after menin knockdown in 3T3-L1 cells showed a 1.5–1.7-fold increase in fat-cell size. Global gene expression analysis of mESC-derived adipocytes showed that lack of menin downregulated the expression of many differentially methylated genes including the tumor suppressor long noncoding RNA Meg3 but upregulated gene expression from the prolactin gene family locus. Our results show that menin deficiency leads to fat-cell hypertrophy and provide model systems that could be used to study the regulation of fat-cell size.


1975 ◽  
Vol 84 (2) ◽  
pp. 221-225 ◽  
Author(s):  
J. D. Wood ◽  
M. B. Enser ◽  
D. J. Restall

SUMMARYIn view of the dependence of fat metabolism on the size of fat cells and the lack of information describing the change in fat cell size which occurs during growth in pigs, an examination was made of the size of subcutaneous fat cells in Pietrain and Large White pigs of 30–95 kg live weight. A microscopic procedure was used and fat cell diameter was measured at two levels in the outer layer of shoulder fat and at two levels in the inner layer.In both breeds the rate at which cell diameter increased in size with live weight was greater in the inner layer than the outer layer. At all levels this rate of increase was greater in Pietrains. At the two levels in the inner layer the cells from Pietrains increased in size by 41% and 54% between 30 and 95 kg live weight and the cells from Large Whites increased in size by 23% and 36%. The result was that at 95 kg live weight both breeds had cells of similar size in the inner layer.Therefore in pigs of the same live weight, cell size varies, depending on the site at which the examination is made and the breed of pig. Even at constant cell size, however, the lipogenic capacity of the fat from different levels and different breeds must be different since the cells increase in size at different rates.


1981 ◽  
Vol 240 (1) ◽  
pp. E72-E78 ◽  
Author(s):  
M. R. Greenwood ◽  
M. P. Cleary ◽  
R. Gruen ◽  
D. Blase ◽  
J. S. Stern ◽  
...  

Young Zucker lean (Fa/-) and obese (fa/fa) female rats were fed the fatty acid synthesis inhibitor (-)-hydroxy-citrate as a dietary admixture for 39 days. In the lean rats, (-)-hydroxycitrate treatment decreased body weight, food intake, percent of body fat, and fat cell size. In the obese rat, food intake and body weight were reduced but the percent of body fat remained unchanged. Throughout the treatment period, obese rats maintained a fat cell size equivalent to their obese controls. Although a reduction in fat cell number in the obese rats occurred during the treatment period, marked hyperplasia was observed during the posttreatment period. The results of this study indicate that the obese rat, despite a substantial reduction in body weight produced by (-)-hydroxycitrate, still defends its obese body composition.


1983 ◽  
Vol 49 (3) ◽  
pp. 411-417 ◽  
Author(s):  
Katherine A. Smalley ◽  
Quinton R. Rogers ◽  
James G. Morris

1. The effects of feeding either high-protein (HP) or low-protein (LP) diets between 1.8 and 15 kg live weight (LW) and a low-energy (LE) or high-energy (HE) intake subsequently on the cellularity of muscle and adipose tissue in pigs growing to 75 kg LW were investigated.2. The effects of the nutritional treatments on muscle tissue were assessed from the weight and DNA content of the m. adductor. For adipose tissue the total DNA content and fat cell size of the subcutaneous adipose tissue contained in the left shoulder joint were determined.3. Feeding the LP diets in early life reduced the weight and DNA content of the m. adductor (P < 0.01) and increased fat cell size (P < 0.01) at 15 kg LW.4. Subsequent to 15 kg there was an almost linear increase in muscle DNA with increasing LW, and the difference between pigs from the initial protein treatments progressively diminished and was no longer apparent at 60 kg LW.5. At 30 kg LW, pigs given the LP diets before 15 kg LW contained less DNA in the subcutaneous adipose tissue from the shoulder joint (P < 0.01) and had larger fat cells (P < 0.05) than pigs given the HP diets initially. However, adipose DNA and fat cell size increased with increasing LW and the differences resulting from the initial protein treatments progressively diminished. On the LE and HE treatments subsequent to 15 kg these differences were no longer evident at 45 and 60 kg respectively.6. Pigs given the HE intake subsequent to 15 kg, contained less DNA in muscle tissue (P < 0·05) at 60 and 75 kg LW and had larger fat cells (P < 0·05) at 45, 60 and 75 kg LW, than pigs on the LE treatment.


2020 ◽  
Vol 21 (18) ◽  
pp. 6836
Author(s):  
Hyo Jin Maeng ◽  
Gha Young Lee ◽  
Jae Hyun Bae ◽  
Soo Lim

Fibroblast growth factor 21 (FGF21) is a hormonal regulator of lipid and glucose metabolism. We aimed to investigate the effect of an FGF21 analogue (LY2405319) on the development of atherosclerosis and its associated parameters. ApoE−/− mice were fed an atherogenic diet for 14 weeks and were randomly assigned to control (saline) or FGF21 (0.1 mg/kg) treatment group (n = 10/group) for 5 weeks. Plaque size in the aortic arch/valve areas and cardiovascular risk markers were evaluated in blood and tissues. The effects of FGF21 on various atherogenesis-related pathways were also assessed. Atherosclerotic plaque areas in the aortic arch/valve were significantly smaller in the FGF21 group than in controls after treatment. FGF21 significantly decreased body weight and glucose concentrations, and increased circulating adiponectin levels. FGF21 treatment alleviated insulin resistance and decreased circulating concentrations of triglycerides, which were significantly correlated with plaque size. FGF21 treatment reduced lipid droplets in the liver and decreased fat cell size and inflammatory cell infiltration in the abdominal visceral fat compared with the control group. The monocyte chemoattractant protein-1 levels were decreased and β-hydroxybutyrate levels were increased by FGF21 treatment. Uncoupling protein 1 expression in subcutaneous fat was greater and fat cell size in brown fat was smaller in the FGF21 group compared with controls. Administration of FGF21 showed anti-atherosclerotic effects in atherosclerosis-prone mice and exerted beneficial effects on critical atherosclerosis pathways. Improvements in inflammation and insulin resistance seem to be mechanisms involved in the mitigation of atherosclerosis by FGF21 therapy.


Metabolism ◽  
1980 ◽  
Vol 29 (3) ◽  
pp. 246-253 ◽  
Author(s):  
R. Gruen ◽  
R. Kava ◽  
M.R.C. Greenwood

1983 ◽  
Vol 49 (1) ◽  
pp. 109-118 ◽  
Author(s):  
R. G. Campbell ◽  
A. C. Dunkin

1. The effects of level of feeding and level of protein in the early postnatal period on the cellularity of subcutaneous adipose tissue and body fat content of pigs were investigated in two experiments.2. In Expt 1, piglets were given a common liquid diet at energy intakes equivalent to 2·8 or 5·2 times energy for maintenance (M) between 1·8 and 6·5 kg live weight (LW), and a common dry diet at 2·8 or 4·5 M between 6·5 and 20 kg LW. Between 20 and 75 kg LW all pigs were given a second dry diet at 4·0 M.3. In both experiments the effects of nutritional treatments on fat cell number at 20 and 75 kg LW (Expt 1) and at 45 kg LW (Expt 2) were assessed by measuring the DNA content of the subcutaneous adipose tissue contained in the left shoulder joint. Fat cell size was assessed in the same tissue by measuring the diameter of collagenase-released adipocytes.4. In Expt 1, raising the level of feeding between 1·8 and 6·5 kg LW increased body fat content and average fat cell diameter at both 6·5 (P < 0·01) and 20 kg LW (P < 0·05) but had no effect on either measurement at 75 kg LW. Similarly, raising the level of feeding between 6·5 and 20 kg LW increased body fat content and fat cell size at both 20 (P < 0·01) and 75 kg LW (P < 0·05). There was an almost twofold increase in the DNA content of subcutaneous adipose tisuue between 20 and 75 kg LW. However, it was not significantly affected at either weight by level of feeding before or subsequent to 6·5 kg LW.5. In Expt 2, reducing the level of dietary protein between 1·8 and 6·5 kg LW increased body fat content (P < 0·01) and fat cell size (P < 0·01) at the latter weight. Although level of dietary protein to 6·5 kg LW had no effect on body fat content or the weight of subcutaneous adipose tissue in the shoulder joint at 45 kg LW, pigs given the lowest-protein diet contained less DNA (P < 0·05) in the subcutaneous adipose tissue and had larger (P < 0·05) fat cells than those given the highest-protein diet to 6·5 kg LW. Reducing the protein content of the diet fed subsequent to 6·5 kg LW increased the body fat content (P < 0·01) and fat cell size (P < 0·01) at 45 kg LW.


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