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<title>Artikuluak-Gastronomia</title>
<link href="https://hdl.handle.net/20.500.11984/477" rel="alternate"/>
<subtitle/>
<id>https://hdl.handle.net/20.500.11984/477</id>
<updated>2026-07-17T12:26:58Z</updated>
<dc:date>2026-07-17T12:26:58Z</dc:date>
<entry>
<title>11-β Hydroxysteroid dehydrogenase type 2 expression in white adipose tissue is strongly correlated with adiposity</title>
<link href="https://hdl.handle.net/20.500.11984/14600" rel="alternate"/>
<author>
<name>Milagro, Fermin I.</name>
</author>
<author>
<name>Campion, Javier</name>
</author>
<author>
<name>Martínez, José A.</name>
</author>
<id>https://hdl.handle.net/20.500.11984/14600</id>
<updated>2026-06-19T06:15:51Z</updated>
<published>2007-01-01T00:00:00Z</published>
<summary type="text">11-β Hydroxysteroid dehydrogenase type 2 expression in white adipose tissue is strongly correlated with adiposity
Milagro, Fermin I.; Campion, Javier; Martínez, José A.
Glucocorticoid action within the cells is regulated by the levels of glucocorticoid receptor (GR) expression and two enzymes, 11-β hydroxysteroid dehydrogenase type 1 (11βHSD1), which converts inactive to active glucocorticoids, and 11-β hydroxysteroid dehydrogenase type 2 (11βHSD2), which regulates the access of active glucocorticoids to the receptor by converting cortisol/corticosterone to the glucocorticoid-inactive form cortisone/dehydrocorticosterone. Male Wistar rats developed obesity by being fed a high-fat diet for 56 days, and GR, 11βHSD1 and 11βHSD2 gene expression were compared with control-diet fed animals. Gene expression analysis of 11βHSD1, 11βHSD2 and GR were performed by RT-PCR in subcutaneous and retroperitoneal adipose tissue. High-fat fed animals overexpressed 11βHSD2 in subcutaneous but not in retroperitoneal fat. Interestingly, mRNA levels strongly correlated in both tissues with different parameters related to obesity, such as body weight, adiposity and insulin resistance, suggesting that this gene is a reliable marker of adiposity in this rat model of obesity. Thus, 11βHSD2 is expressed in adipose tissue by both adipocytes and stromal-vascular cells, which suggests that this enzyme may play an important role in preventing fat accumulation in adipose tissue.
</summary>
<dc:date>2007-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Weight gain induced by high-fat feeding involves increased liver oxidative stress</title>
<link href="https://hdl.handle.net/20.500.11984/14599" rel="alternate"/>
<author>
<name>Milagro, Fermin I.</name>
</author>
<author>
<name>Campion, Javier</name>
</author>
<author>
<name>Martínez, José A.</name>
</author>
<id>https://hdl.handle.net/20.500.11984/14599</id>
<updated>2026-06-19T06:15:51Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">Weight gain induced by high-fat feeding involves increased liver oxidative stress
Milagro, Fermin I.; Campion, Javier; Martínez, José A.
Objective: To assess the effects of high-fat feeding on white adipose tissue gene expression and liver oxidative stress.Research Methods and Procedures: Male Wistar rats were fed on standard pelleted or high-fat diet to produce a diet-induced obesity model. Therefore, body composition, serum biochemical values and liver malondialdehyde (MDA) were determined after 56 days of feeding. Expression (mRNA) values of three genes were also determined by reverse transcriptase-polymerase chain reaction in white adipose tissue.Results: Animals fed on the high-fat diet showed more body weight, higher fat deposition and total liver weight, and increased energy intake compared with those on the standard-fat diet. Serum fasting measurements (glucose, insulin, leptin) and homeostasis model assessment insulin resistance index were significantly increased by the high-fat diet consumption. As an indicator of oxidative stress, peroxide decomposition in liver was analyzed, showing an increase of MDA concentrations in rats fed on high-fat diet in comparison with control rats. Interestingly, liver MDA levels correlated positively with body weight gain, serum leptin, and homeostasis model assessment. Finally, leptin and glycerol-3-phosphate dehydrogenase mRNA levels, but not fatty acid synthase, were increased by high-fat diet in comparison with the control-fed group.Discussion: These results show a link among increased fat depots, insulin resistance, and liver oxidative stress. Thus, liver oxidative stress probably contributes to hepatic disorders and aggravates the metabolic syndrome, which is accompanied by a stimulation of the esterification of fatty acids as measured by glycerol-3-phosphate dehydrogenase in the adipose tissue, providing support to the hypothesis that not only calories count in the induction of weight gain or metabolic syndrome and that other factors such as oxidative stress may be involved.
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Epinephrine-Induced Reduction in Insulin Receptor mRNA Level and Stability in U-937 Human Promonocytic Cells</title>
<link href="https://hdl.handle.net/20.500.11984/14596" rel="alternate"/>
<author>
<name>Mas, Antonio</name>
</author>
<author>
<name>Campion, Javier</name>
</author>
<author>
<name>Aller, Patricio</name>
</author>
<author>
<name>calle, consuelo</name>
</author>
<id>https://hdl.handle.net/20.500.11984/14596</id>
<updated>2026-06-19T06:15:52Z</updated>
<published>1998-01-01T00:00:00Z</published>
<summary type="text">Epinephrine-Induced Reduction in Insulin Receptor mRNA Level and Stability in U-937 Human Promonocytic Cells
Mas, Antonio; Campion, Javier; Aller, Patricio; calle, consuelo
The administration of 10-5 M epinephrine transiently decreased insulin receptor (IR) mRNA levels in U-937 human promonocytic cells, which reached their minimum value after 24 hours. Such a decrease seems to be due, at least in part, to a reduction in transcript stability, since the IR mRNA half-life was observed to decline from approximately 4 h in untreated cells to 3 h in epinephrine-treated cells. Computer inspection of the sequence of the 3′ untranslated region of the human IR mRNA showed nine AUUUA pentamers and three U-rich regions. These domains could be targets for a RNA-binding protein induced by treatment with epinephrine producing a destabilization of IR mRNA in U-937 cells.
</summary>
<dc:date>1998-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>In vivo tissue specific modulation of rat insulin receptor gene expression in an experimental model of mineralocorticoid excess</title>
<link href="https://hdl.handle.net/20.500.11984/14595" rel="alternate"/>
<author>
<name>Campion, Javier</name>
</author>
<author>
<name>Lahera, Vicente</name>
</author>
<author>
<name>Cachofeiro, Victoria</name>
</author>
<author>
<name>Maestro, Begoña</name>
</author>
<author>
<name>dávila, norma</name>
</author>
<author>
<name>Carranza, María del Carmen</name>
</author>
<author>
<name>calle, consuelo</name>
</author>
<id>https://hdl.handle.net/20.500.11984/14595</id>
<updated>2026-06-19T06:15:49Z</updated>
<published>1998-01-01T00:00:00Z</published>
<summary type="text">In vivo tissue specific modulation of rat insulin receptor gene expression in an experimental model of mineralocorticoid excess
Campion, Javier; Lahera, Vicente; Cachofeiro, Victoria; Maestro, Begoña; dávila, norma; Carranza, María del Carmen; calle, consuelo
Insulin receptor (IR) gene expression at the mRNA level was investigated in hindlimb skeletal muscle, epididymal adipose&#13;
tissue and in the liver of rats exposed to prolonged in vivo administration of deoxycorticosterone acetate (DOCA). Following&#13;
treatment, plasma insulin levels were reduced while glucose levels increased compared to values in control rats. DOCA-treated&#13;
animals showed an increase in blood pressure and a reduction in body weight. This treatment also induced hypokalemia and&#13;
decreased plasma protein levels. Sodium levels were unaffected. Moreover, no differences in DNA and protein content or in&#13;
the indicator of cell size (protein/DNA) were observed in the skeletal muscle or adipose tissue of animals. In contrast, there&#13;
was a clear increase in the protein and DNA contents of the liver with no change in the indicator of cell size. Northern blot&#13;
assays revealed 2 major IR mRNA species of approximately 9.5 and 7.5 Kb in the 3 tissues from control animals. DOCA treatment&#13;
induced no change in the levels of either RNA species in skeletal muscle. However, a decrease of approximately 22% was&#13;
detected in the levels of both species in adipose tissue whereas the liver showed an increase of 64%. These results provide the&#13;
first evidence for an in vivo tissue-specific modulation of IR mRNA levels under experimental conditions of mineralocorticoid&#13;
excess.
</summary>
<dc:date>1998-01-01T00:00:00Z</dc:date>
</entry>
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