Effect of fasting on insulin receptor-related receptor messenger ribonucleic acid in rat kidney

Chrysis, Dionisios; Moats-Staats, BM; Le, Underwood

doi:10.1677/joe.0.159r009

Cited by 8 publications

(5 citation statements)

References 21 publications

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“…The PCR protocol for PPARg consisted of 2 min of denaturing at 95C, followed by 30 cycles with 95C denaturing for 0 s, 55C annealing for 5 s and 72C extension for 35 s. b-Actin was used as a control to account for any variations due to efficiencies of the reverse transcription and PCR. In the present study, b-actin was not found to be significantly different across treatment, results which are in line with previous studies showing that it remains stable under fasting conditions [8,25]. The PCR protocol for b-actin consisted of 2 min of denaturing at 95C, followed by 30 cycles with 95C denaturing for 0 s, 60C annealing for 5 s and 72C extension for 12 s. Detection of the fluorescent product was carried out at the end of the 72C extension period.…”

Section: Real-time Quantitative Pcrsupporting

confidence: 93%

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARγ and key enzymes of lipid oxidation

Samec

Seydoux

Russell

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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The uncoupling protein homologs UCP2 and UCP3 have been proposed as candidate genes for the regulation of lipid metabolism. Within the context of this hypothesis, we have compared, from fed and fasted rats, changes in gene expression of skeletal muscle UCP2 and UCP3 with those of carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase, two key enzymes regulating lipid flux across the mitochondrial beta-oxidation pathway. In addition, changes in gene expression of peroxisome proliferator-activated receptor gamma, a nuclear transcription factor implicated in lipid metabolism, were also investigated. The results indicate that in response to fasting, the mRNA levels of UCP2, UCP3, carnitine palmitoyltransferase I and medium-chain acyl-CoA dehydrogenase are markedly increased, by three- to sevenfold, in the gastrocnemius and tibialis anterior (fast-twitch muscles, predominantly glycolytic or oxidative-glycolytic), but only mildly increased, by less than twofold, in the soleus (slow-twitch muscle, predominantly oxidative). Furthermore, such muscle-type dependency in fasting-induced transcriptional changes in UCP2, UCP3, carnitine palmitoyltransferase and medium-chain acyl-CoA dehydrogenase persists when the increase in circulating levels of free fatty acids during fasting is abolished by the anti-lipolytic agent nicotinic acid - with blunted responses only in the slow-twitch muscle contrasting with unabated increases in fast-twitch muscles. Independently of muscle type, however, the mRNA levels of peroxisome proliferator-activated receptor gamma are not altered during fasting. Taken together, these studies indicate a close association between fasting-induced changes in UCP2 and UCP3 gene expression with those of key regulators of lipid oxidation, and are hence consistent with the hypothesis that these UCP homologs may be involved in the regulation of lipid metabolism. Furthermore, they suggest that in response to fasting, neither the surge of free fatty acids in the circulation nor induction of the peroxisome proliferator-activated receptor gamma gene may be required for the marked upregulation of genes encoding the UCP homologs and key enzymes regulating lipid oxidation in fast-twitch muscles.

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Section: Real-time Quantitative Pcrsupporting

confidence: 93%

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARγ and key enzymes of lipid oxidation

Samec

Seydoux

Russell

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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“…Riboprobes were prepared by in vitro transcription and purified on 5% acrylamide/8 m urea gel. RPA were carried out as previously described (Chrysis et al ., 1998). Briefly, 20 µg total brain RNA was hybridized overnight at 45 °C with biotin‐labeled riboprobes (nestin and cyclophilin).…”

Section: Methodsmentioning

confidence: 99%

In vivo effects of insulin‐like growth factor‐I (IGF‐I) on prenatal and early postnatal development of the central nervous system

Popken

Hodge

et al. 2004

Eur J of Neuroscience

156

128

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The in vivo actions of insulin-like growth factor-I (IGF-I) on prenatal and early postnatal brain development were investigated in transgenic (Tg) mice that overexpress IGF-I prenatally under the control of regulatory sequences from the nestin gene. Tg mice demonstrated increases in brain weight of 6% by embryonic day (E) 18 and 27% by postnatal day (P) 12. In Tg embryos at E16, the volume of the cortical plate was significantly increased by 52% and total cell number was increased by 54%. S-phase labeling with 5-bromo-2'-deoxyuridine revealed a 13-15% increase in the proportion of labeled neuroepithelial cells in Tg embryos at E14. In Tg mice at P12, significant increases in regional tissue volumes were detected in the cerebral cortex (29%), subcortical white matter (52%), caudate-putamen (37%), hippocampus (49%), dentate gyrus (71%) and habenular complex (48%). Tg mice exhibited significant increases in the total number of neurons in the cerebral cortex (27%), caudate-putamen (27%), dentate gyrus (69%), medial habenular nucleus (61%) and lateral habenular nucleus (36%). In the cerebral cortex and subcortical white matter of Tg mice, the total numbers of glial cells were significantly increased by 37% and 42%, respectively. The numerical density of apoptotic cells in the cerebral cortex, labeled by antibodies against active caspase-3, was reduced by 26% in Tg mice at P7. Our results demonstrate that IGF-I can both promote proliferation of neural cells in the embryonic central nervous system in vivo and inhibit their apoptosis during postnatal life.

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“…RPA was performed as reported previously (Chrysis et al, 1998). Briefly, 20 g samples of CB total RNA were hybridized overnight at 45°C with biotin-labeled riboprobes (3 fmol of cyclophilin, 2.5 fmol of Bcl-x and Bax, or 3 fmol of cyclophilin, 3 fmol of Bad, and 2 fmol of Bcl-2).…”

Section: Methodsmentioning

confidence: 99%

Insulin-Like Growth Factor-I Overexpression Attenuates Cerebellar Apoptosis by Altering the Expression of Bcl Family Proteins in a Developmentally Specific Manner

2001

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In studies of transgenic (Tg) mice that overexpress insulin-like growth factor-I (IGF-I) exclusively in the CNS, we demonstrated a dramatic increase in cerebellar granule cell number that appeared to be attributable predominantly to enhanced survival. IGF-I anti-apoptotic actions are well established in cultured neurons, but comparable studies in vivo are few. Using the same Tg mice, therefore, we set out to document IGF-I antiapoptotic effects during cerebellar development and to probe IGF-I signaling mechanisms. Compared with cerebella (CBs) of non-Tg littermates, those of Tg mice had fewer apoptotic cells at postnatal day 7 (P7) and showed a similar tendency at P14 and P21. At each age studied, procaspase-3 and caspase-3 were decreased in CBs of Tg mice. The caspase-3 decline was accompanied by decreases in the 85 kDa fragment of Poly(ADP-ribose) polymerase, a known product of caspase cleavage, suggesting decreased caspase activity. At P7 decreased apoptosis in Tg mice was associated with increased expression of the anti-apoptotic Bcl genes, Bcl-x L and Bcl-2. The mRNA expression of the proapoptotic Bcl genes, Bax and Bad, also was increased, but no changes were observed in the abundance of their proteins. At P14 Bcl-xL and Bcl-2 expression were similar in normal and Tg mice; Bax mRNA was unchanged in Tg mice, but its protein abundance was decreased, and both Bad mRNA and protein abundance were decreased. At P21 Bcl-xL and Bcl-2 expression were unchanged, but Bax and Bad expression were decreased. Our data show that IGF-I exerts anti-apoptotic actions during cerebellar development, and thereby alters the magnitude of naturally occurring apoptosis. IGF-I appears to affect multiple steps in the apoptotic pathway in a developmentally specific manner. IGF-I decreases caspase-3 availability and activity, increases the expression of anti-apoptotic Bcl-x L and Bcl-2 during early postnatal development, and decreases proapoptotic Bax and Bad expression at later developmental stages.

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Effect of fasting on insulin receptor-related receptor messenger ribonucleic acid in rat kidney

Cited by 8 publications

References 21 publications

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARγ and key enzymes of lipid oxidation

Skeletal muscle heterogeneity in fasting-induced upregulation of genes encoding UCP2, UCP3, PPARγ and key enzymes of lipid oxidation

In vivo effects of insulin‐like growth factor‐I (IGF‐I) on prenatal and early postnatal development of the central nervous system

Insulin-Like Growth Factor-I Overexpression Attenuates Cerebellar Apoptosis by Altering the Expression of Bcl Family Proteins in a Developmentally Specific Manner

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