Fucoxanthin regulates adipocytokine mRNA expression in white adipose tissue of diabetic/obese KK-Ay mice

2010 ◽  
Vol 504 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Masashi Hosokawa ◽  
Tatsuya Miyashita ◽  
Sho Nishikawa ◽  
Shingo Emi ◽  
Takayuki Tsukui ◽  
...  
Endocrinology ◽  
2005 ◽  
Vol 146 (12) ◽  
pp. 5631-5636 ◽  
Author(s):  
Hitoshi Ando ◽  
Hayato Yanagihara ◽  
Yohei Hayashi ◽  
Yuri Obi ◽  
Shuichi Tsuruoka ◽  
...  

Various peripheral tissues show circadian rhythmicity, which is generated at the cellular level by their own core oscillators that are composed of transcriptional/translational feedback loops involving a set of clock genes. Although the circulating levels of some adipocytokines, i.e. bioactive substances secreted by adipocytes, are on a 24-h rhythmic cycle, it remains to be elucidated whether the clock gene system works in adipose tissue. To address this issue, we investigated the daily mRNA expression profiles of the clock genes and adipocytokines in mouse perigonadal adipose tissues. In C57BL/6J mice, all transcript levels of the clock genes (Bmal1, Per1, Per2, Cry1, Cry2, and Dbp) and adipocytokines (adiponectin, resistin, and visfatin) clearly showed 24-h rhythms. On the other hand, the rhythmic expression of these genes was mildly attenuated in obese KK mice and greatly attenuated in more obese, diabetic KK-Ay mice. Obese diabetes also diminished the rhythmic expression of the clock genes in the liver. Interestingly, a 2-wk treatment of KK and KK-Ay mice with pioglitazone impaired the 24-h rhythmicity of the mRNA expression of the clock genes and adipocytokines despite the antidiabetic effect of the drug. In contrast, pioglitazone improved the attenuated rhythmicity in the liver. These findings suggest that the intracellular clock gene system acts in visceral adipose tissues as well as liver and is influenced by the conditions of obesity/type 2 diabetes and pioglitazone treatment.


2018 ◽  
Vol 22 (2) ◽  
pp. 265-272 ◽  
Author(s):  
Y. V. Piskunova ◽  
A. Y. Kazantceva ◽  
A. V. Baklanov ◽  
N. M. Bazhan

The lethal yellow mutation in agouti loci (Ay mutation) reduces the activity of melanocortin (MC) receptors and causes hyperphagia, obesity and type two diabetes mellitus in aging mice (Ay mice). It is unknown if changes in distinct elements of the metabolic system such as white adipose tissue (WAT) and brown adipose tissue (BAT), and skeletal muscle will manifest before the development of obesity. The aim of this work was to measure the relative gene expression of key proteins that regulate carbohydrate-lipid metabolism in WAT, BAT and skeletal muscle in Ay mice before the development of obesity. C57Bl/6J mice bearing a dominant autosomal mutation Ay (Ay /a mice) and mice of the standard genotype (a/a mice, control) have been studied in three age groups: 10, 15 and 30 weeks. The relative mRNA level of genes was measured by real-time PCR in skeletal muscles (uncoupling protein 3 (Ucp3) and carnitine palmitoyl transferase 1b (Cpt1b) (free fatty acids oxidation), solute carrier family 2 (facilitated glucose transporter), member 4 (Slc2a4) (glucose uptake)), in WAT lipoprotein lipase (Lpl) (triglyceride deposition), hormone-sensitive lipase (Lipe) (lipid mobilization), and Slc2a4 (glucose uptake)), and in BAT: uncoupling protein 1 (Ucp1) (energy expenditure). The expression of Cpt1b was reduced in young Ay mice (10 weeks), there was no transient peak of transcription of Cpt1b, Ucp3 in skeletal muscle tissue and Lipe, Slc2a4 in WAT in early adult Ay mice (15 weeks), which was noted in а/а mice. Reduction of the transcriptional activity of the studied genes in skeletal muscle and white adipose tissue can initiate the development of melanocortin obesity in Ay mice.


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


2014 ◽  
Vol 145 (3) ◽  
pp. 490-498 ◽  
Author(s):  
Zhuo-Si Li ◽  
Kenji Noda ◽  
Eriko Fujita ◽  
Yuki Manabe ◽  
Takashi Hirata ◽  
...  

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.


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