Down-regulation of AMP-activated protein kinase by calorie restriction in rat liver

To, Kazuo; Yamaza, Haruyoshi; Komatsu, Toshimitsu; Hayashida, Takahiro; Hayashi, Hiroko; Toyama, Hiroaki; Chiba, Takuya; Higami, Yoshikazu; Shimokawa, Isao

doi:10.1016/j.exger.2007.07.003

Cited by 37 publications

(21 citation statements)

References 22 publications

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“…Activation of the adiponectin-AMPKα pathway in skeletal muscle might occur via an insulin-independent mechanism for improved glucose tolerance and whole body insulin resistance following CR. However, we and others have been unable to confirm the upregulation of p-AMPKα in skeletal muscle following CR (Gonzalez et al 2004;To et al 2007). …”

Section: Discussioncontrasting

confidence: 71%

Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner

Park

Komatsu

Hayashi

et al. 2008

AGE

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Calorie restriction (CR) may exert an antiaging effect through a metabolic adaptation to limited energy intake. The present study investigated the effect of CR on insulin signaling in response to glucose load in the epididymal adipose tissue of male F344 rats at 7 and 22 months of age. Young and middle-aged rats were fed ad libitum (AL) or 30% CR diets for 4 months, underwent glucose tolerance tests and were sacrificed 15 min after an intraperitoneal glucose or saline injection to evaluate glucose-stimulated insulin response and subsequent activation of insulin signaling molecules in the adipose tissue. In the 7-and 22-month AL groups, glucose administration increased serum insulin levels and also increased phosphorylated (p) levels of the insulin receptor (IR), v-akt murine thymoma viral oncogene homolog (Akt), protein kinase C (PKC) ζ/λ and the membrane fraction of glucose transporter 4 (mGlut4). In contrast, in the 7-month CR group, p-Akt, p-PKCζ/λ and mGlut4 levels were upregulated without glucose stimulation; the glucose load augmented the p-IR level but there was no additional activation of the downstream molecules. In the 22-month CR group, these unexpected findings were not observed. In summary, basal levels of insulin signaling molecules such as p-Akt, p-PKCζ/λ, and mGlut4 were significantly increased with a low insulin response in the 7-month CR group. The present results suggest the presence of an age-specific insulin-independent mechanism that is induced by CR to regulate energy metabolism in white adipose tissue.

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Section: Discussioncontrasting

confidence: 71%

Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner

Park

Komatsu

Hayashi

et al. 2008

AGE

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“…Additionally, no changes were detected with caloric restriction in AMPK activation or Sirt1 protein. While there is considerable evidence pointing to a key role of AMPK and Sirt1 in promoting the beneficial effects of caloric restriction, several studies do not support this, reporting no change in the activation of these factors following this intervention (Gonzalez et al, 2004; To et al, 2007). Moreover, we expected that the combination of caloric restriction and resveratrol would produce an additive or even a synergistic effect on these mitochondrial regulatory proteins since global gene expression profiling comparing the specific intracellular effects of both caloric restriction and resveratrol in aging mice revealed a partial overlap between the two treatments (Barger et al, 2008; Pearson et al, 2008).…”

Section: Discussionmentioning

confidence: 96%

Short-term caloric restriction, resveratrol, or combined treatment regimens initiated in late-life alter mitochondrial protein expression profiles in a fiber-type specific manner in aged animals

Joseph

Malamo

Silvestre

et al. 2013

Experimental Gerontology

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Aging is associated with a loss in muscle known as sarcopenia that is partially attributed to apoptosis. In aging rodents, caloric restriction (CR) increases health and longevity by improving mitochondrial function and the polyphenol resveratrol (RSV) has been reported to have similar benefits. In the present study, we investigated the potential efficacy of using short-term (6 weeks) CR (20%), RSV (50 mg/kg/day), or combined CR + RSV (20% CR and 50 mg/kg/day RSV), initiated at late-life (27 months) to protect muscle against sarcopenia by altering mitochondrial function, biogenesis, content, and apoptotic signaling in both glycolytic white and oxidative red gastrocnemius muscle (WG and RG, respectively) of male Fischer 344 × Brown Norway rats. CR but not RSV attenuated the age-associated loss of muscle mass in both mixed gastrocnemius and soleus muscle, while combined treatment (CR + RSV) paradigms showed a protective effect in the soleus and plantaris muscle (P < 0.05). Sirt1 protein content was increased by 2.6-fold (P < 0.05) in WG but not RG muscle with RSV treatment, while CR or CR + RSV had no effect. PGC-1α levels were higher (2-fold) in the WG from CR-treated animals (P < 0.05) when compared to ad-libitum (AL) animals but no differences were observed in the RG with any treatment. Levels of the anti-apoptotic protein Bcl-2 were significantly higher (1.6-fold) in the WG muscle of RSV and CR + RSV groups compared to AL (P < 0.05) but tended to occur coincident with elevations in the pro-apoptotic protein Bax so that the apoptotic susceptibility as indicated by the Bax to Bcl-2 ratio was unchanged. There were no alterations in DNA fragmentation with any treatment in muscle from older animals. Additionally, mitochondrial respiration measured in permeabilized muscle fibers was unchanged in any treatment group and this paralleled the lack of change in cytochrome c oxidase (COX) activity. These data suggest that short-term moderate CR, RSV, or CR + RSV tended to modestly alter key mitochondrial regulatory and apoptotic signaling pathways in glycolytic muscle and this might contribute to the moderate protective effects against aging-induced muscle loss observed in this study.

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“…29 In mice, caloric restriction downregulates AMPK activity in the liver. 30 Activation of LKB1/AMPK and inhibition of mTOR (mammalian target of rapamycin) contribute to the premature aging phenotype of Zmpste24 Ϫ/Ϫ mice. 27 AMPK hyperactivation has also been reported in the skeletal muscle and liver of old rodents.…”

Section: Discussionmentioning

confidence: 99%

SIRT1 Promotes Proliferation and Prevents Senescence Through Targeting LKB1 in Primary Porcine Aortic Endothelial Cells

Liu

Lee

et al. 2010

Circulation Research

260

217

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Under conditions that cause endothelium injury, such as hypertension, high cholesterol levels and turbulent blood flow, replication of endothelial cells is increased for regenerating the damaged endothelium. 3 However, the regenerated endothelial cells usually reach replicative senescence after a finite number of cell replication. Senescent endothelial cells show diminished vasomotor-regulatory activities and elevated expression of proinflammatory molecules, which contribute to the development of age-associated cardiovascular diseases, such as atherosclerosis. 4 SIRT1 is a class III deacetylase implicated in a wide range of cellular functions. 5 This protein has attracted enormous interest since the discovery of the potential antiaging activities of its yeast homolog, Sir2. In mammalian system, the beneficial activities of SIRT1 against aging diseases, such as those related to neuro-and cardioprotection, have been suggested by many studies. 5,6 Cardiovascular aging represents the largest portion of age-related morbidity and mortality. Therefore, it is particularly important to elucidate whether SIRT1 exerts any antiaging effects in the cardiovascular system.

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Down-regulation of AMP-activated protein kinase by calorie restriction in rat liver

Cited by 37 publications

References 22 publications

Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner

Calorie restriction initiated at a young age activates the Akt/PKCζ/λ-Glut4 pathway in rat white adipose tissue in an insulin-independent manner

Short-term caloric restriction, resveratrol, or combined treatment regimens initiated in late-life alter mitochondrial protein expression profiles in a fiber-type specific manner in aged animals

SIRT1 Promotes Proliferation and Prevents Senescence Through Targeting LKB1 in Primary Porcine Aortic Endothelial Cells

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