Modulation of IGFBP2 mRNA Expression in White Adipose Tissue upon Aging and Obesity

2010 ◽  
Vol 42 (11) ◽  
pp. 787-791 ◽  
Author(s):  
Z. Li ◽  
F. Picard
2010 ◽  
Vol 504 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Masashi Hosokawa ◽  
Tatsuya Miyashita ◽  
Sho Nishikawa ◽  
Shingo Emi ◽  
Takayuki Tsukui ◽  
...  

Endocrinology ◽  
2003 ◽  
Vol 144 (8) ◽  
pp. 3547-3554 ◽  
Author(s):  
Takayuki Masaki ◽  
Go Yoshimichi ◽  
Seiichi Chiba ◽  
Tohru Yasuda ◽  
Hitoshi Noguchi ◽  
...  

Abstract To examine the functional role of CRH in the regulation of energy homeostasis by leptin, we measured the effects of the CRH antagonist, α-helical CRH 8–41 (αCRH) on a number of factors affected by leptin activity. These included food intake, body weight, hypothalamic c-fos-like immunoreactivity (c-FLI), weight and histological characterization of white adipose tissue, and mRNA expressions of uncoupling protein (UCP) in brown adipose tissue (BAT) in C57Bl/6 mice. Central infusion of leptin into the lateral cerebroventricle (icv) caused significant induction of c-FLI in the paraventricular nucleus (PVN), ventromedial hypothalamic nucleus (VMH), dorsomedial hypothalamic nucleus, and arcuate nucleus. In all these nuclei, the effect of leptin on expression of cFLI in the PVN and VMH was decreased by treatment with αCRH. Administration of leptin markedly decreased cumulative food intake and body weight with this effect being attenuated by pretreatment with αCRH. In peripheral tissue, leptin up-regulated BAT UCP1 mRNA expression and reduced fat depositions in this tissue. Those changes in BAT were also decreased by treatment with αCRH. As a consequence of the effects on food intake or energy expenditure, treatment with αCRH attenuated the leptin-induced reduction of body adiposity, fat cell size, triglyceride contents, and ob mRNA expression in white adipose tissue. Taken together, these results indicate that CRH neurons in the PVN and VMH may be an important mediator for leptin that contribute to regulation of feeding, adiposity, and UCP expression.


1994 ◽  
Vol 130 (2) ◽  
pp. 146-150 ◽  
Author(s):  
Giovanni De Pergola ◽  
Xuefan Xu ◽  
Björn Carlsson ◽  
Peter Eriksson ◽  
Staffan Edén ◽  
...  

De Pergola G, Xu X, Carlsson B, Eriksson P, Edén S, Giorgino R, Björntorp P. Estradiol regulation of mRNA expression of stimulatory α-subunit in white adipose tissue from female rats. Eur J Endocrinol 1994;130:146–50. ISSN 0804–4643 Adipose tissue has been recognized as a major peripheral metabolic target of estrogens. The present study was addressed to examine in female rats whether differences in the adipose tissue mRNA expression of α-subunit of stimulatory (Gs) and/or inhibitory (Gj) G-proteins exist between intact and ovariectomized rats, the latter with or without estradiol or testosterone treatment. The fat cell membrane protein amount of Gs and Gj α-subunit also was examined. All these parameters were evaluated in parametrial fat tissue samples obtained from 40 female Sprague-Dawley rats. A group of rats (N=20) was investigated for evaluation of mRNA expression and another group (N=20) for quantification of the protein amount of Gs and Gj α-subunit. Each group was represented by five control rats (sham-operated), five ovariectomized (OVX) rats, five ovariectomized rats treated with estradiol (OVXE) and five ovariectomized rats treated with testosterone (OVXT). Ribonucleic acid extracted from adipose tissue and analyzed by northern blot with Gαs, Gαi-1 and Gαi-2 cRNA probes revealed three major bands with estimated sizes of 1.9, 3.5 and 2.35 kb, respectively. Messenger RNA quantitative analysis, by a solution of hybridization RNAase protection assay on total nucleic acid samples, showed that the amount of Gαi-1 and Gαi-2 mRNA was similar within the different groups, whereas the Gαs mRNA was significantly less abundant (p <0.01) in OVX and OVXT rats than in control or OVXE rats. No difference in Gαs mRNA content was found between control and OVXE rats. As with mRNA analysis, protein quantitative analysis by an enzyme-linked immunosorbent assay in fat cell membrane preparation showed that the amount of Gαi(1–2) was similar within the different groups and that the Gαs content was significantly higher in control and OVXE rats than in OVX and OVXT rats (p<0.01). This study in female rats shows that estradiol may be involved in the control of protein amount and mRNA expression of Gs α-subunit in adipose tissue. These results may explain in part how estrogens regulate the variations of body fat mass in female rats. Giovanni De Pergola, via Putignani 236, 70122 Bari, Italy


2021 ◽  
Vol 23 (1) ◽  
pp. 257
Author(s):  
Barbara Gawronska-Kozak ◽  
Katarzyna Walendzik ◽  
Sylwia Machcinska ◽  
Artur Padzik ◽  
Marta Kopcewicz ◽  
...  

Dermal white adipose tissue (dWAT) is involved in the maintenance of skin homeostasis. However, the studies concerning its molecular regulation are limited. In the present paper, we ask whether the introduction of two transcription factors, Foxn1 and Hif-1α, into the post-wounded skin of Foxn1-/- mice regulates dWAT during wound healing (days 3 and 6). We have chosen lentivirus vectors (LVs) as a tool to deliver Foxn1 and Hif-1α into the post-wounded skin. We documented that combinations of both transgenes reduces the number, size and diameter of dermal adipocytes at the wound bed area. The qRT-PCR analysis of pro-adipogenic genes, revealed that LV-Hif-1α alone, or combined with LV-Foxn1, increases the mRNA expression of Pparγ, Glut 4 and Fasn at post-wounding day 6. However, the most spectacular stimulatory effect of Foxn1 and/or Hif-1α was observed for Igf2, the growth factor participating in adipogenic signal transduction. Our data also shows that Foxn1/Hif-1α, at post-wounding day 3, reduces levels of CD68 and MIP-1γ mRNA expression and the percentage of CD68 positive cells in the wound site. In conclusion, the present data are the first to document that Foxn1 and Hif-1α cooperatively (1) regulate dWAT during the proliferative phase of skin wound healing through the Igf2 signaling pathway, and (2) reduce the macrophages content in the wound site.


2005 ◽  
Vol 130 (1-2) ◽  
pp. 97-103 ◽  
Author(s):  
Tetsuo Tsubone ◽  
Takayuki Masaki ◽  
Isao Katsuragi ◽  
Katsuhiro Tanaka ◽  
Tetsuya Kakuma ◽  
...  

2008 ◽  
Vol 101 (2) ◽  
pp. 197-205 ◽  
Author(s):  
Georgios A. Papadopoulos ◽  
Tim Erkens ◽  
Dominiek G. D. Maes ◽  
Luc J. Peelman ◽  
Theo A. T. G. van Kempen ◽  
...  

The aim of this study was to describe the effects of two diets differing in n-6:n-3 ratio and prepartal feeding regime on gene expression of PPARγ1a/1b, PPARγ1c/1d, PPARγ2, PPARγ coactivator 1A (PPARGC1A), GLUT4, TNFα, adiponectin, leptin, leptin receptor (LEPR), fatty acid binding protein 4 (FABP4), lipoprotein lipase (LPL) in sows' white adipose tissue on the first day of lactation. The relationship between mRNA expression of these genes and circulating insulin, leptin and thyroid hormones was also considered. Diets contained a low (supplemented with fish oil; f group) or a high (supplemented with sunflower oil; s group) n-6:n-3 ratio and were provided from 8 (f8, s8) or 3 d (f3, s3) before parturition (onset day 8 or 3). A low n-6:n-3 ratio reduced the 1 d postpartum expression of PPARγ2 and PPARGC1A but only when applied from 3 d before parturition. Circulating leptin was negatively correlated with mRNA expression of adiponectin, LEPR and LPL, whereas thyroxine was positively correlated with levels of PPARGC1A. In conclusion, the effect of dietary treatments, e.g. altering the n-6:n-3 ratio, around parturition on the expression of crucial genes in nutrient metabolism can be modulated by the duration of application before parturition.


2010 ◽  
Vol 299 (5) ◽  
pp. C1162-C1170 ◽  
Author(s):  
Zhongxiao Wan ◽  
A. Brianne Thrush ◽  
Melanie Legare ◽  
Bruce C. Frier ◽  
Lindsey N. Sutherland ◽  
...  

Fatty acid reesterification in adipose tissue is dependent on the generation of glycerol 3-phosphate, and, at least in rodent adipose tissue, this appears to occur primarily through glyceroneogenesis. A key enzyme in this process is pyruvate dehydrogenase kinase 4 (PDK4). PDK4 is induced in white adipose tissue by thiazolidinediones (TZDs) and the inhibition or knockdown of PDK4 inhibits TZD-induced increases in glyceroneogenesis. Since TZDs have many unwanted side effects, we were interested in identifying alternative mechanisms that could regulate PDK4 mRNA expression in white adipose tissue. In this regard we hypothesized that exercise, fasting, and epinephrine would increase PDK4 mRNA levels in rat epididymal adipose tissue. We further postulated that the p38 mitogen-activated protein kinase (MAPK) and 5′-AMP-activated protein kinase (AMPK) signaling pathways would control PDK4 mRNA expression in cultured adipose tissue. Exercise, fasting, and in or ex vivo epinephrine treatment increased PDK4 mRNA levels. These perturbations did not increase the expression of PDK1, -2, or -3. Pyruvate dehydrogenase phosphorylation was increased after an overnight fast and 4 h after the cessation of exercise. In cultured adipose tissue, epinephrine increased p38 and AMPK signaling; however, the direct activation of AMPK by AICAR or metformin led to reductions in PDK4 mRNA levels. The p38 inhibitor SB202190 reduced epinephrine-mediated increases in p38 MAPK activation without altering hormone-sensitive lipase or AMPK phosphorylation or attenuating epinephrine-induced increases in lipolysis. Reductions in p38 MAPK signaling were associated with decreases in PDK4 mRNA expression. The inhibition of peroxisome proliferator-activated receptor-γ (PPARγ) also attenuated the induction of PDK4. Our results are the very first to demonstrate an epinephrine-mediated regulation of PDK4 mRNA levels in white adipose tissue and suggest that p38 MAPK and PPARγ could be involved in this pathway.


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