Up-regulation of rat adipose tissue adiponectin gene expression by long-term but not by short-term food restriction

Turyn, Jacek; Korczyńska, Justyna; Presler, Malgorzata; Stelmańska, Ewa; Goyke, Elżbieta; Świerczyński, Julian

doi:10.1007/s11010-008-9733-5

Cited by 15 publications

(10 citation statements)

References 38 publications

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“…Moreover, this was associated with significantly increased serum adiponectin concentration ( Table 1). These data confirm the results reported recently [28]. The results presented in Table 3 …”

Section: Resultssupporting

confidence: 93%

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

et al. 2011

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Corticosterone — product of 11-β-hydroxysteroid dehydrogenase type I (11βHSD1) stimulates adipocytes differentiation and activates lipogenic enzymes gene expression in white adipose tissue (WAT) of rats. The aim of the study was to examine the effect of chronic food restriction, often practised by obese individuals trying to lose body mass, on: a) 11βHSD1 gene expression, b) expression of genes associated with adipocyte differentiation (PPARg, SREBP-1, adiponectin), and c) expression of genes associated with lipogenesis in WAT of rats. Two-month old rats were divided into a control and a food restricted group obtaining 50% of food consumed by controls for 30 days. mRNA levels of studied genes in perirenal WAT were analysed by real-time PCR. 11βHSD1 and lipogenic enzymes activities were measured by radiometric conversion assay and by spectrophotometric assay respectively. Food restriction caused significant increase of 11βHSD1, PPARg, SREBP1, adiponectin and lipogenic enzymes mRNA levels in perirenal WAT. 11βHSD1 and some lipogenic enzymes activities were also increased by food restriction. The coordinated up-regulation of 11βHSD1, and genes associated with adipocyte differentiation and lipogenesis by food restriction suggests that such nutritional condition shifts WAT metabolism, that would permit this tissue to synthesize and accumulate triacylglycerols immediately after refeeding.

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Section: Resultssupporting

confidence: 93%

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

et al. 2011

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“…This sustained effect is relevant for interpreting the present study in which p38 and JNK phosphorylation was elevated both in muscle frozen immediately after removal (gastrocnemius) and in isolated muscles (epitrochlearis and soleus) incubated ex vivo without added corticosterone for 50 min were greater for the CR versus the AL rats. CR has been shown by others to increase plasma adiponectin concentration (55,58,74). This adipokine can induce the activation of p38 in cultured myocytes (38,70,71).…”

Section: R133mentioning

confidence: 88%

Improved insulin sensitivity with calorie restriction does not require reduced JNK1/2, p38, or ERK1/2 phosphorylation in skeletal muscle of 9-month-old rats

Sharma¹,

Bhat²,

Kassa³

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Sharma N, Bhat AD, Kassa AD, Xiao Y, Arias EB, Cartee GD. Improved insulin sensitivity with calorie restriction does not require reduced JNK1/2, p38, or ERK1/2 phosphorylation in skeletal muscle of 9-month-old rats. Am J Physiol Regul Integr Comp Physiol 302: R126 -R136, 2012. First published October 19, 2011 doi:10.1152/ajpregu.00372.2011.-Calorie restriction [CR; ϳ40% below ad libitum (AL) intake] improves the health of many species, including rats, by mechanisms that may be partly related to enhanced insulin sensitivity for glucose disposal by skeletal muscle. Excessive activation of several mitogen-activated protein kinases (MAPKs), including JNK1/2, p38, and ERK1/2 has been linked to insulin resistance. Although insulin can activate ERK1/2, this effect is not required for insulin-mediated glucose uptake. We hypothesized that skeletal muscle from male 9-mo-old Fischer 344/Brown Norway rats CR (35-40% beginning at 3 mo old) versus AL rats would have 1) attenuated activation of JNK1/2, p38, and ERK1/2 under basal conditions; and 2) no difference for insulin-induced ERK1/2 activation. In contrast to our hypothesis, there were significant CR-related increases in the phosphorylation of p38 (epitrochlearis, soleus, and gastrocnemius), JNK1 (epitrochlearis and soleus), and JNK2 (gastrocnemius). Consistent with our hypothesis, CR did not alter insulin-mediated ERK1/2 activation. The greater JNK1/2 and p38 phosphorylation with CR was not attributable to diet effects on muscle oxidative stress (assessed by protein carbonyls and 4-hydroxynonenal protein conjugates). In muscles from the same rats used for the present study, we previously reported a CR-related increase in insulin-mediated glucose uptake by the epitrochlearis and the soleus (Sharma N, Arias EB, Bhat AD, Sequea DA, Ho S, Croff KK, Sajan MP, Farese RV, Cartee GD. Am J Physiol Endocrinol Metab 300: E966 -E978, 2011). The present results indicate that the improved insulin sensitivity with CR is not attributable to attenuated MAPK phosphorylation in skeletal muscle.

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“…[44]–[46] However, the reduction in adiponectin levels might take longer to occur, as the stimulatory effect of caloric restriction on adiponectin gene expression was only detectable after long-term caloric restriction and not after short-term restriction. [47] …”

Section: Discussionmentioning

confidence: 99%

Changes in Gene Expression Associated with FTO Overexpression in Mice

et al. 2014

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Single nucleotide polymorphisms in the first intron of the fat-mass-and-obesity-related gene FTO are associated with increased body weight and adiposity. Increased expression of FTO is likely underlying this obesity phenotype, as mice with two additional copies of Fto (FTO-4 mice) exhibit increased adiposity and are hyperphagic. FTO is a demethylase of single stranded DNA and RNA, and one of its targets is the m6A modification in RNA, which might play a role in the regulation of gene expression. In this study, we aimed to examine the changes in gene expression that occur in FTO-4 mice in order to gain more insight into the underlying mechanisms by which FTO influences body weight and adiposity. Our results indicate an upregulation of anabolic pathways and a downregulation of catabolic pathways in FTO-4 mice. Interestingly, although genes involved in methylation were differentially regulated in skeletal muscle of FTO-4 mice, no effect of FTO overexpression on m6A methylation of total mRNA was detected.

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Up-regulation of rat adipose tissue adiponectin gene expression by long-term but not by short-term food restriction

Cited by 15 publications

References 38 publications

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

Chronic food restriction up-regulates 11-β-hydroxysteroid dehydrogenase

Improved insulin sensitivity with calorie restriction does not require reduced JNK1/2, p38, or ERK1/2 phosphorylation in skeletal muscle of 9-month-old rats

Changes in Gene Expression Associated with FTO Overexpression in Mice

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