Adipose tissue-specific increase in angiotensinogen expression and secretion in the obese (fa/fa) Zucker rat

2002 ◽  
Vol 282 (1) ◽  
pp. E59-E66 ◽  
Author(s):  
Isabelle Hainault ◽  
Guillaume Nebout ◽  
Sophie Turban ◽  
Bernadette Ardouin ◽  
Pascal Ferré ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Zucker Rats ◽  
Fat Cell ◽  
Cell Content ◽  
Tissue Specific ◽  
Genotype Effect ◽  
Obese Rats ◽  
Specific Increase ◽  
Adipocyte Hypertrophy

We investigated angiotensinogen (AGT) expression in adipose tissue and liver of Zucker rats during the onset of obesity. The developmental pattern of AGT expression (protein and mRNA) in liver was similar in both genotypes. In inguinal adipose tissue, AGT cell content was similar in suckling and weaned pups in lean rats, whereas it continuously increased with age in obese rats. AGT amount in adipocytes was unaffected by the genotype until weaning. Thereafter, adipocytes from obese rats displayed a significant increase in AGT content that was strengthened with age. Compared with the cell content, the amount of secreted AGT over 24 h was higher, and a genotype effect was observed as early as 14 days of age. Using fat cell populations differing by size, we showed that this AGT oversecretion was not solely related to adipocyte hypertrophy. Our results demonstrate that the fa genotype exerts a control on the production of AGT in a tissue-specific manner, suggesting a local role of AGT in the overdevelopment of adipose tissue.

scholarly journals Adipose-tissue-specific increase in glyceraldehyde-3-phosphate dehydrogenase activity and mRNA amounts in suckling pre-obese Zucker rats. Effect of weaning

1988 ◽  
Vol 254 (2) ◽  
pp. 483-487 ◽  
Author(s):  
I Dugail ◽  
A Quignard-Boulange ◽  
R Bazin ◽  
X Le Liepvre ◽  
M Lavau
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Zucker Rats ◽  
Tissue Specific ◽  
Gapdh Gene ◽  
Gapdh Activity ◽  
Weanling Rats ◽  
Obese Rats ◽  
Specific Increase ◽  
Obese Zucker Rats

The regulation of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene expression was studied during the onset of obesity in the genetically obese (fa/fa) rat by determination of GAPDH activity and hybridizable mRNA amounts in adipose tissue and liver from suckling and weanling rats. GADPH activity remained low throughout the suckling period, and a burst of activity occurred after weaning in both lean and obese pups. As early as 7 days of age, adipose tissue from pre-obese rats displayed a significant increase in enzyme activity, whereas no difference could be detected in the liver. In both suckling (16 days of age) and weanling (30 days of age) obese rats a proportionate increase in GAPDH activity and mRNA amounts was observed in adipose tissue, but not in liver. It is concluded that the obese genotype influences GAPDH gene expression at a pretranslational level and in a tissue-specific manner. This phenomenon could partly contribute to the hyperactive fat accretion in the obese rat, since glycolysis is the major metabolic pathway for lipogenic substrates in adipose tissue.

Association of fat cell size and paracrine growth factors in development of hyperplastic obesity

1998 ◽  
Vol 275 (6) ◽  
pp. R1898-R1908 ◽  
Author(s):  
Brenda G. Marques ◽  
Dorothy B. Hausman ◽  
Roy J. Martin
Keyword(s):  
Adipose Tissue ◽  
Growth Factors ◽  
Conditioned Medium ◽  
Cellular Proliferation ◽  
Cell Number ◽  
Zucker Rats ◽  
Fat Cell ◽  
Obese Rats ◽  
Paracrine Growth Factors ◽  
Obese Zucker Rats

Inguinal, epididymal, and retroperitoneal adipose tissue from lean and obese Zucker rats, 3–15 wk of age, was used to determine the association among adipocyte size distribution, the presence of paracrine growth factors in adipose tissue, and subsequent changes in adipocyte number. For each specific depot and time point, obese rats had a greater percentage of large adipocytes than did lean rats. A positive correlation ( P < 0.02) was found in obese rats between the percentage of inguinal and epididymal adipocytes in the 140- to 180-μm size range and the ability of conditioned medium prepared from these depots to stimulate cellular proliferation in a bioassay system utilizing preadipocytes from inguinal fat pads of normal rats. Proliferative activity of the conditioned medium from all depots in obese rats was positively correlated ( P < 0.01) to subsequent changes in fat cell number. The data presented here for the inguinal and epididymal depot of obese Zucker rats are consistent with the hypothesis that enlarged adipocytes secrete growth factors that induce preadipocyte proliferation.

scholarly journals Transglutaminases and Obesity in Humans: Association of F13A1 to Adipocyte Hypertrophy and Adipose Tissue Immune Response

2020 ◽  
Vol 21 (21) ◽  
pp. 8289
Author(s):  
Mari T. Kaartinen ◽  
Mansi Arora ◽  
Sini Heinonen ◽  
Aila Rissanen ◽  
Jaakko Kaprio ◽  
...  
Keyword(s):  
Immune Response ◽  
Adipose Tissue ◽  
Family Members ◽  
Enrichment Analysis ◽  
Human Adipose Tissue ◽  
Adipocyte Size ◽  
Gene Enrichment ◽  
Adipocyte Hypertrophy ◽  
Mz Twins

Transglutaminases TG2 and FXIII-A have recently been linked to adipose tissue biology and obesity, however, human studies for TG family members in adipocytes have not been conducted. In this study, we investigated the association of TGM family members to acquired weight gain in a rare set of monozygotic (MZ) twins discordant for body weight, i.e., heavy–lean twin pairs. We report that F13A1 is the only TGM family member showing significantly altered, higher expression in adipose tissue of the heavier twin. Our previous work linked adipocyte F13A1 to increased weight, body fat mass, adipocyte size, and pro-inflammatory pathways. Here, we explored further the link of F13A1 to adipocyte size in the MZ twins via a previously conducted TWA study that was further mined for genes that specifically associate to hypertrophic adipocytes. We report that differential expression of F13A1 (ΔHeavy–Lean) associated with 47 genes which were linked via gene enrichment analysis to immune response, leucocyte and neutrophil activation, as well as cytokine response and signaling. Our work brings further support to the role of F13A1 in the human adipose tissue pathology, suggesting a role in the cascade that links hypertrophic adipocytes with inflammation.

Relationship of adipocyte size to hyperphagia in developing male obese Zucker rats

1992 ◽  
Vol 262 (1) ◽  
pp. R33-R38 ◽  
Author(s):  
J. R. Vasselli ◽  
J. A. Fiene ◽  
C. A. Maggio
Keyword(s):  
Adipose Tissue ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Lipoprotein Lipase Activity ◽  
Adipocyte Size ◽  
High Fat ◽  
Obese Rats ◽  
Obese Zucker Rats ◽  
Relationship Of ◽  
Cumulative Intake

In growing male obese Zucker rats, hyperphagia reaches a maximum or “breakpoint” and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 micrograms lipid), while that of chow-fed obese rats only approached maximal at 20 wk (0.81 microgram lipid). At these time points, lipoprotein lipase activity paralleled adipocyte size. These data indicate that the duration of the growing obese rat's hyperphagia coincides with adipocyte filling and suggest the existence of feeding stimulatory and inhibitory signals from adipose tissue.

scholarly journals Enhanced nutritionally induced adipose tissue development in mice with stromelysin-1 gene inactivation

2003 ◽  
Vol 89 (04) ◽  
pp. 696-704 ◽  
Author(s):  
Erik Maquoi ◽  
Diego Demeulemeester ◽  
Gabor Vörös ◽  
Désire Collen ◽  
H. Lijnen
Keyword(s):  
Adipose Tissue ◽  
Research Society ◽  
The Body ◽  
Tissue Development ◽  
Cholesterol Levels ◽  
Fat Deposits ◽  
Adipose Tissue Development ◽  
Adipocyte Hypertrophy ◽  
Deficient Mice

SummaryTo investigate a potential role of stromelysin-1 (MMP-3) in development of adipose tissue, 5 week old male MMP-3 deficient mice (MMP-3-/-) and wild-type (MMP-3+/+) controls were kept on a high fat diet (HFD) for 15 weeks. MMP-3-/- mice were hyperphagic and gained more weight than the MMP-3+/+ mice. At the time of sacrifice, the body weight of the MMP-3-/- mice was significantly higher than that of the MMP-3+/+ mice, as was the weight of the isolated subcutaneous (SC) and gonadal (GON) fat deposits. Significant adipocyte hypertrophy was observed in the GON but not in the SC adipose tissue of MMP-3-/- mice. Fasting plasma glucose and cholesterol levels were comparable in both genotypes, whereas triglyceride levels were significantly lower in MMP-3-/- mice. Staining with an endothelial cell specific lectin revealed a significantly higher blood vessel density and larger total stained area in the GON adipose tissues of MMP-3-/- mice. Thus, in a murine model of nutritionally induced obesity, MMP-3 impairs adipose tissue development, possibly by affecting food intake and/or adipose tissue-related angiogenesis.Theme paper: Part of this paper was originally presented at the joint meetings of the 16th International Congress of the International Society of Fibrinolysis and Proteolysis (ISFP) and the 17th International Fibrinogen Workshop of the International Fibrinogen Research Society (IFRS) held in Munich, Germany, September, 2002.

scholarly journals Gene expression of lipid storage-related enzymes in adipose tissue of the genetically obese Zucker rat. Co-ordinated increase in transcriptional activity and potentiation by hyperinsulinaemia

1992 ◽  
Vol 281 (3) ◽  
pp. 607-611 ◽  
Author(s):  
I Dugail ◽  
A Quignard-Boulangé ◽  
X Le Liepvre ◽  
B Ardouin ◽  
M Lavau
Keyword(s):  
Adipose Tissue ◽  
Mrna Level ◽  
Lipid Storage ◽  
Zucker Rats ◽  
Transcriptional Level ◽  
Transcription Rate ◽  
Mrna Levels ◽  
Zucker Rat ◽  
Obese Zucker Rat ◽  
Obese Rats

The genetically obese Zucker rat displays excessive fat storage capacity which is due to a tissue-specific increase in the activities of a number of lipid storage-related enzymes in adipose tissue. The aim of this study was to investigate the molecular mechanism responsible for this phenomenon. Lean (Fa/fa) and obese (fa/fa) Zucker rats were studied during the early stages of adipose tissue overdevelopment, both before (at 16 days of age) and after (at 30 days of age) the emergence of hyperinsulinaemia, in order to delineate the effects of the fatty genotype independently of those of hyperinsulinaemia. Lipoprotein lipase (LPL), glycerophosphate dehydrogenase (GPDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and malic enzyme (ME) mRNA levels in the adipose tissue of lean and obese rats were assessed by Northern blot analysis, and the relative transcription rates of the corresponding genes were compared in the two genotypes by a nuclear run-on assay. In normoinsulinaemic 16-day-old pre-obese rats, mRNA levels were increased over control values (LPL, 5-fold; ME, 2-fold; GAPDH, 3-fold), in close correlation with genotype-mediated differences in enzyme activities. Stimulation of the transcription rates of the ME and GAPDH genes was observed in obese rats, which could fully account for differences in steady-state mRNA levels. At this age, GPDH activity, mRNA level and transcription rate were similar in the two genotypes. In hyperinsulinaemic 30-day-old obese rats, a 6-7-fold increase in both mRNA and the transcription rate of GPDH emerged, together with an amplification of the genotype-mediated differences observed in younger animals (GAPDH, 6-fold; ME, 7.9-fold; LPL, 10-fold). These results demonstrate that the obese genotype exerts a co-ordinated control on the expression of these genes in adipose tissue, mainly at the transcriptional level. This genotype effect is greatly amplified by the development of hyperinsulinaemia.

Increased islet blood flow in obese rats: role of the autonomic nervous system

1992 ◽  
Vol 262 (5) ◽  
pp. E736-E740 ◽  
Author(s):  
N. Atef ◽  
A. Ktorza ◽  
L. Picon ◽  
L. Penicaud
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Ventromedial Hypothalamus ◽  
Zucker Rats ◽  
Islet Blood Flow ◽  
Obese Rats ◽  
Increased Sensitivity ◽  
Obese Zucker Rats

Hyperinsulinemia, a main feature of both human and animal obesity, has been demonstrated to be due to both an increased sensitivity to nutrient secretagogues and an impairment of the nervous regulation of insulin secretion. Recent studies have shown that pancreatic islet blood flow increases under conditions associated with an enhanced insulin secretion. The aim of this study was to determine whether or not changes in islet blood flow are present in hyperinsulinemic obese rats. Using the nonradioactive microsphere technique, we were able to show a significantly higher islet blood flow in obese rats either of the Zucker strain or Wistar rats after lesion of the ventromedial hypothalamus than in their respective lean controls. Subdiaphragmatic vagotomy had no significant effect on basal islet blood flow of lean rats, whereas it decreased significantly that of obese Zucker rats. Conversely, clonidine, an alpha 2-adrenergic agonist, induced a higher decrease of islet blood flow in obese than in lean Zucker rats. The injection of an intravenous bolus of glucose (375 mg/kg iv) increased significantly more islet blood flow in obese than in lean Zucker rats. It is concluded that obese rats present an increased pancreatic islet blood flow, which may result, at least in part, from exaggerated parasympathetic activity and lower than normal sympathetic activity. This could participate in the hyperinsulinemia observed in these rats.

Mechanisms of increased lipoprotein lipase in fat cells of obese Zucker rats

1991 ◽  
Vol 261 (5) ◽  
pp. E653-E660 ◽  
Author(s):  
S. K. Fried ◽  
I. J. Turkenkopf ◽  
I. J. Goldberg ◽  
M. H. Doolittle ◽  
T. G. Kirchgessner ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Lipoprotein Lipase ◽  
Bovine Milk ◽  
Zucker Rats ◽  
Fat Cells ◽  
Fat Cell ◽  
Cell Basis ◽  
Rat Adipocytes ◽  
Obese Rats ◽  
Obese Zucker Rats

The mechanisms underlying the increased activity of lipoprotein lipase (LPL) in adipocytes of genetically obese Zucker rats was studied. Relative rates of LPL synthesis (percent of total protein synthesis) determined by biosynthetic labeling and specific immunoprecipitation were similar in isolated fat cells from lean and obese rats, in the absence or presence of insulin. Insulin stimulated LPL synthesis as a result of a general increase in protein synthesis, and this effect was more marked in the obese fat cells. Levels of LPL mRNA, as a percent of total RNA, were also similar in fat cells from lean and obese rats. In contrast, when the data are calculated on a per fat cell basis, rates of LPL synthesis per fat cell are ninefold higher in obese compared with lean cells, accounting for the increase in LPL activity per fat cell. Fat cells from lean and obese rats showed similar rates of binding and degradation of purified bovine milk 125I-labeled LPL per unit fat cell surface area. Thus, on a per cell basis, rates of LPL turnover are increased in enlarged Zucker rat adipocytes, but there is no specific abnormality in the cellular regulation of LPL. Increases in LPL activity in obese rat adipocytes are related to an overall hyperresponsiveness to insulin effects on protein synthesis.

Effect of swim training on development of obesity in the genetically obese rat

1982 ◽  
Vol 242 (3) ◽  
pp. R204-R211 ◽  
Author(s):  
J. L. Walberg ◽  
P. A. Mole ◽  
J. S. Stern
Keyword(s):  
Body Composition ◽  
Food Restriction ◽  
Plasma Insulin ◽  
Cell Number ◽  
Skeletal Growth ◽  
Zucker Rats ◽  
Fat Cell ◽  
Full Development ◽  
Obese Rats ◽  
Obese Zucker Rats

Seven-week-old female lean and obese Zucker rats were swim trained or kept sedentary for 8 wk. Another group of obese rats was exercised plus food restricted. During exercise training, obese and lean rats ate more but gained less body weight than sedentary controls. Exercise favorably altered body composition, adipose cellularity, and plasma insulin of the obese rat. Exercise plus food restriction more dramatically affected body composition and adipose cellularity but was no more effective in depressing hyperinsulinemia than exercise alone. Following 8 wk of retirement, dorsal fat cell number remained depressed to formerly exercised obese rats whereas adipose cellularity in other depots, body composition, and plasma insulin were similar to control levels. Thus, exercise delayed but did not prevent the full development of obesity in the Zucker rat. Food restriction along with exercise resulted in more permanent effects on adipose cellularity than exercise alone but stunted muscle and skeletal growth.

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