Specific increase in leptin production in obese (falfa) rat adipose cells

In the obese state, enlarged adipose cells display an altered gene-expression profile and metabolic capacity. The aim of this study was to gain insight into their secretory function, by assessing two secreted proteins, leptin and angiotensinogen, in adipose cells of obese (fa/fa) Zucker rats. A marked and co-ordinate increase in leptin mRNA, gene transcription and promoter activity was observed in obese compared with lean (Fa/fa) rat adipose cells, and this resulted in increased leptin release in culture. Two sets of observations suggest that this effect is due to the fa mutation. First, adipose-cell leptin release was higher in heterozygous (Fa/fa) than in homozygous (Fa/Fa) lean rats. Second, leptin release was not enhanced in enlarged adipose cells of FalFa rats fed a high-fat diet for 15 days. At variance with leptin, angiotensinogen production was not significantly increased in the obese cells. Dexamethasone stimulated both leptin and angiotensinogen release in lean and obese rat adipose cells. The magnitude of leptin stimulation was higher in fa/fa than in Fa/fa rats, whereas angiotensinogen release was increased to the same extent in both genotypes. These observations suggest that leptin production is specifically enhanced in enlarged adipose cells of obese Zucker rats and that cell hypertrophy is not the sole determinant of this feature. Increased leptin production might be related to disruption of leptin signalling by the fa mutation.

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Adipsin mRNA amounts are not decreased in the genetically obese Zucker rat

Biochemical Journal ◽

10.1042/bj2570917 ◽

1989 ◽

Vol 257 (3) ◽

pp. 917-919 ◽

Cited By ~ 16

Author(s):

I Dugail ◽

X Le Liepvre ◽

A Quignard-Boulangé ◽

J Pairault ◽

M Lavau

Keyword(s):

Gene Expression ◽

High Fat Diet ◽

Zucker Rats ◽

Zucker Rat ◽

Obese Mice ◽

High Fat ◽

Adult Rats ◽

Obese Zucker Rat ◽

Obese Rats ◽

Obese Zucker Rats

Adipsin gene expression as assessed by mRNA amounts was examined in adipose tissue of genetically obese rats at the onset (16 days of age) or at later stages (30 and 60 days of age) of obesity. Amounts of mRNA were equivalent in obese and lean rats at 16 days of age. In adult rats, we observed a 2-fold decrease in adipsin mRNA in the obese rats compared with control lean rats, which was abolished by weaning the animals on a high-fat diet. Our data show that, in sharp contrast with genetically obese mice, adipsin mRNA is not suppressed in genetically obese Zucker rats.

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Maternal high-fat diet associated with altered gene expression, DNA methylation, and obesity risk in mouse offspring

PLoS ONE ◽

10.1371/journal.pone.0192606 ◽

2018 ◽

Vol 13 (2) ◽

pp. e0192606 ◽

Cited By ~ 40

Author(s):

Madeline Rose Keleher ◽

Rabab Zaidi ◽

Shyam Shah ◽

M. Elsa Oakley ◽

Cassondra Pavlatos ◽

...

Keyword(s):

Gene Expression ◽

Dna Methylation ◽

High Fat Diet ◽

Obesity Risk ◽

High Fat ◽

Altered Gene Expression ◽

Altered Gene

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Mature adipocytes and perivascular adipose tissue stimulate vascular smooth muscle cell proliferation: effects of aging and obesity

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01259.2004 ◽

2005 ◽

Vol 289 (5) ◽

pp. H1807-H1813 ◽

Cited By ~ 97

Author(s):

Christine Barandier ◽

Jean-Pierre Montani ◽

Zhihong Yang

Keyword(s):

Adipose Tissue ◽

Smooth Muscle ◽

Growth Factor ◽

Smooth Muscle Cell ◽

Conditioned Medium ◽

High Fat Diet ◽

Zucker Rats ◽

High Fat ◽

Perivascular Adipose Tissue ◽

Obese Zucker Rats

Adipocytes and perivascular adipose tissue are emerging as regulators of vascular function. The effects of adipocytes and perivascular adipose tissue on human smooth muscle cell (SMC) proliferation were investigated. Conditioned medium was prepared from cultured premature and differentiated 3T3-L1 adipocytes and from periaortic adipose tissue from young (3 mo) and old (24 mo) Wistar-Kyoto (WKY) rats, lean and obese Zucker rats (3 mo), and WKY rats fed normal chow or a high-fat diet for 3 mo. Conditioned medium from differentiated (but not premature) adipocytes stimulated SMC proliferation, which was abolished by charcoal and proteinase K treatment but was resistant to heat, trypsin, or phospholipase B (to hydrolyze lysophosphatidic acid). Further experiments demonstrated that the growth factor(s) are hydrosoluble and present in the fraction of molecular mass >100 kDa. Moreover, conditioned medium from periaortic adipose tissue stimulated SMC proliferation, which was significantly enhanced in aged rats and in rats fed a high-fat diet but not in obese Zucker rats deficient in functional leptin receptors. In conclusion, mature adipocytes release hydrosoluble protein growth factor(s) with a molecular mass >100 kDa for SMCs. Perivascular adipose tissue stimulates SMC proliferation, which is enhanced in aged WKY and in high-fat, diet-induced obesity but not in leptin receptor-deficient obese Zucker rats. These adipocyte-derived growth factor(s) and the effect of perivascular adipose tissue may be involved in vascular disease associated with aging and obesity.

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