Dexamethasone Regulates Obese Expression in Isolated Rat Adipocytes

Murakami, Tohru; Iida, Mitsuru; Shima, Keiji

doi:10.1006/bbrc.1995.2422

Cited by 195 publications

(135 citation statements)

References 0 publications

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…Glucocorticoids are known to increase leptin mRNA levels both in vivo (8,9) and in isolated primary adipocytes (9,11). The finding that this stimulation is, in large part, independent of de novo protein synthesis (9) suggests that glucocorticoids may directly activate transcription of the leptin gene. Glucocorticoid does not, however, significantly up-regulate leptin mRNA in 3T3-L1 adipocytes (O.A.M., unpublished results, and ref.…”

Section: Resultsmentioning

confidence: 99%

“…The obese gene is expressed only by adipocytes (1), so the choices are limited to isolated adipocytes or to established preadipocyte cell lines, e.g., the 3T3-L1 and 3T3-F442A lines, that can be induced to differentiate into adipocytes in culture. Although the expression of leptin by isolated adipocytes is responsive to certain physiological agents, such as cAMP elevating agents and glucocorticoids (8,9,11), these cells are not well suited for promoter analysis because they are difficult to transfect and fail to maintain their differentiated characpreadipocytes. The level of expression leptin mRNA and mRNAs encoding other adipocyte markers was determined by Northern blot analysis of total RNA isolated from fat pads derived from the implanted preadipocytes described in Proc.…”

Section: Discussionmentioning

confidence: 99%

“…Insulin (6,7), glucocorticoid (8,9), and certain endotoxins and cytokines (10) potently up-regulate expression of the gene whereas cAMP and ␤-adrenergic agonists down-regulate its expression (11,12). In ob͞ob mice, which possess a mutated obese gene, and in db͞db mice, which possess a mutated leptin receptor gene, the obese gene is markedly overexpressed (6).…”

mentioning

confidence: 99%

“…Although adipocytes in primary culture have proven useful in identifying exogenous agents (e.g., hormones) that affect leptin expression (8,9), these cells lose their capacity to express leptin when carried in culture and, therefore, are of limited use for promoter analysis. We have sought to develop a methodology by which the obese gene promoter, as well as other adipocyte gene promoters, can be analyzed in a more appropriate adipose tissue context.…”

mentioning

confidence: 99%

See 3 more Smart Citations

Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3-F442A preadipocytes

Mandrup

Loftus

MacDougald

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

137

132

View full text Add to dashboard Cite

ABSTRACT3T3-F442A preadipocytes implanted s.c. into athymic mice develop into fat pads that are indistinguishable from normal adipose tissue. Implanted preadipocytes harboring a ␤-galactosidase transgene gave rise to fat pads in which almost all adipocytes expressed ␤-galactosidase. This finding proved that the implanted 3T3-F442A preadipocytes, rather than endogenous preadipose cells, gave rise to the newly developed ''adipose tissue.'' 3T3-F442A preadipocytes, when differentiated into adipocytes in cell culture, express the obese gene at an unexpectedly low level, i.e., <1% the level in adipose tissue. However, adipose tissue derived from s.c. implanted 3T3-F442A preadipocytes expressed leptin mRNA at a level comparable to that in epididymal adipose tissue. These findings indicate that a factor(s) or condition, present in the tissue context and necessary for maximal obese gene expression, is lacking in cell culture. Furthermore, adipocytes derived from the implanted cells were hormonally responsive in that leptin mRNA levels were up-regulated 3-to 8-fold by glucocorticoid injection into the host animal. Thus, these findings indicate that adipose-specific promoter-reporter constructs, transfected into 3T3-F442A preadipocytes, can be tested in an in vivo context during and after development of these cells into adipose tissue. Furthermore, the effect of transgenes on the adipogenic development of the implanted preadipocytes can be assessed. Thus, this approach offers a faster and less costly alternative to the transgenic mouse method for assessing adipose gene function.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3-F442A preadipocytes

Mandrup

Loftus

MacDougald

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

137

132

View full text Add to dashboard Cite

show abstract

“…The leptin gene expression has been known to respond to hormones and metabolic state (21,22). The ob/ob mice, which have a R105term nonsense mutation, exhibit a 20-fold increased leptin RNA level (3), suggesting existence of an intact mechanism to sense adiposity and to transcribe the leptin gene.…”

Section: Promoter Analysismentioning

confidence: 99%

Genomic Structure and Promoter Analysis of the Bovine Leptin Gene

et al. 2002

View full text Add to dashboard Cite

SummaryThe product of the leptin gene is a 16-kDa protein secreted by adipose tissue and regulates adiposity. The leptin gene could be a potential candidate gene controlling some proportion of adipose and lean accretion in cattle, and thus, may be referred to as one of genetic factor controlling meat quality determinants such as marbling. We have isolated the bovine leptin gene including its promoter region. We have determined the exon-intron organization of the bovine leptin gene, which consisted of three exons and two introns and spanned about 18.

show abstract

Dexamethasone stimulates leptin release from human adipocytes: Unexpected inhibition by insulin

et al. 1997

View full text Add to dashboard Cite

In the present study we have examined the effect of dexamethasone on ob gene mRNA expression and leptin release from isolated human subcutaneous adipocytes. Dexamethasone stimulated leptin release from cultured adipocytes in a time- and dose-dependent manner. A two-fold increase in leptin release was detectable by 36 h of treatment with 10(-7) M dexamethasone. Leptin release was preceded by a significant 83 +/- 30% increase in ob mRNA after 24 h exposure to the compound. Co-incubation of cells with dexamethasone (10(-7) M) and insulin (10(-7) or 10(-9) M) completely blocked the dexamethasone-stimulated increase in ob mRNA and leptin release. These data demonstrate that insulin and glucocorticoids regulate leptin synthesis and release from human adipocytes in vitro.

show abstract

Dexamethasone Regulates Obese Expression in Isolated Rat Adipocytes

Cited by 195 publications

References 0 publications

Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3-F442A preadipocytes

Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3-F442A preadipocytes

Genomic Structure and Promoter Analysis of the Bovine Leptin Gene

Dexamethasone stimulates leptin release from human adipocytes: Unexpected inhibition by insulin

Contact Info

Product

Resources

About