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Caloric restriction is the only non-genetic manipulation of animals that reliably increases lifespan via an effect on the rate of ageing. The effects of CR are so convincing in animal studies that already some people have started to voluntarily restrict their intake in the hope that they too will increase their lifespans.

Roy Walford's calorie restriction site. Walford was one of the researchers that went in the Biosphere 2 project in Ariziona where he spent 2 years in involuntary restriction. He emerged and continued restricting his intake and wrote several books on the power of CR to increase lifespan. Furthermore, we found no significant effect of BMR on survival, although female survival tended to decrease with increasing BMR.

The whole body BMR is essentially determined by the metabolic intensity and mass of all tissues and organs of the body. Hence, the age dependent decline in BMR observed in our zebra finches could potentially be a result of changes in body composition, e. The mass of various internal organs have previously been found to be a significant predictor for BMR in passerines [35] , but as we conducted a longitudinal study we could not sacrifice birds to obtain information needed to determine if changes in body composition contributed to the metabolic decline observed.

Decreased metabolic intensity with age would be expected if antioxidant defence and repair systems are inadequate to counteract oxidative damage which can impair mitochondrial function [36] , [11]. According to the disposable soma theory [26] a small short-lived bird with a fast life history strategy, such as the zebra finch, is from an evolutionary point of view not expected to invest much energy in mechanisms for somatic maintenance and repair.

Consequently, depending on a relationship between aerobe metabolism and ROS production, oxidative damage would be expected to accumulate with age in a rate determined by total energy metabolism. In the present study we found no association between rates of metabolic ageing and BMR.

We did not investigate other parameters of ageing in our zebra finches. However, in a study of another passerine species, the great tit, Bouwhuis et al.

1. SIRT1 in hepatic glucose and lipid metabolism

It has been argued that when investigating the association between metabolism and the rate of ageing, BMR may not be the best measure of energy metabolism [9]. This because BMR represents an animal's maintenance cost, e. Therefore, if BMR is to be related to the amount of ROS produced through aerobic metabolism, this metabolic trait has to be correlated to the total energy production.

After the introduction of doubly labelled water techniques, daily energy expenditure DEE has become a common metabolic measure which serves as a good indicator for total energy production. However, a significant relationship between DEE and BMR has been found in captive zebra finches [39] during the nonbreeding state. Because the birds in the present study spent most of their life in the nonbreeding state, our BMR measurements should be a good indicator for total energy production and consequently ROS production. Thus, the fact that we found no relationship between intensity of BMR and metabolic decrease with age indicates that different rates of accumulation of oxidative damage is probably not a factor explaining the differences in metabolic ageing observed between individual zebra finches in our study.

According to the free radical theory loss of functionality due to accumulated oxidative damage will ultimately lead to death, and metabolism should therefore be an important factor in determining lifespan. Consequently, we would expect survival to decrease with increasing BMR. We found no relationship between BMR and male survival. Female survival on the other hand tended to decrease with increasing BMR, but the effect failed to reach significance.

However, although the effect of BMR on survival appeared to be slightly stronger in the females the effect did not differ significantly between the sexes. Thus, based on our data we have to conclude that the effect of BMR on the rate of functional deterioration, if any, was not strong enough to significantly influence survival in the zebra finches.

2. SIRT1 in fat cell maturation and fat accumulation

Hence, our results on the relationship between metabolism and survival seem to be inconsistent with the free radical theory. This finding is supported by results obtained at the interspecific level in studies by Montgomery et al. A cold induced acute increase in metabolism was not found to increase plasma oxidative stress levels in zebra finches [42].

Energy and Metabolism Explained

Thus, our use of metabolism as an index of oxidative stress in the zebra finches may be questionable and a more detailed study with actual measurements of oxidative stress is needed in order to make a firm conclusion. We also need to emphasize that the present study was conducted in captive zebra finches living quite sedentary lives with only one or two short breeding periods and they did probably not experience the oxidative challenges they would in the wild.

Increased breeding effort is associated with increased oxidative stress [43] and decreased antioxidant defense [44] in the zebra finch, and as our birds spent most of their lives not breeding this could have decreased the rate of ageing and enhanced survival. An important factor influencing survival was sex, with males showing a higher survival rate than females.

Males had lower BMR than females, but as we found no evidence for a linear relationship between BMR and survival the difference in survival rate was probably not attributed to differences in BMR per se.

Table of Contents for: Energy metabolism and lifespan determina

Anyway, longer lifespans among males is often observed in passerine birds [45] and our results hence support these observations. In conclusion, our study shows that zebra finches experienced metabolic ageing, and that the rate of metabolic ageing was independent of the intensity of BMR. Furthermore, apart from a non-significant tendency in the females, we did not find survival to decrease with increasing BMR.

Based on these findings our study does not support the free radical theory of ageing. However, given the likely complex relationship between metabolism, ROS and antioxidant protection, additional longitudinal studies with quantification of oxidative stress parameters in addition to metabolic measurements are needed to confirm our conclusion. We are grateful to O. Indset, B. Simensen and voluntary students for providing the housing condition for the zebra finches. This work was supported by grants from the Research Council of Norway, nos. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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PLoS One. Published online Sep Berntsen , 3 Elin Noreen , 3 and Claus Bech 3. Henrik H. Author information Article notes Copyright and License information Disclaimer. Competing Interests: The authors have declared that no competing interests exist. Received Jan 6; Accepted Sep 2. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

This article has been cited by other articles in PMC.

Abstract The relationship between energy metabolism and ageing is of great interest because aerobic metabolism is the primary source of reactive oxygen species which is believed to be of major importance in the ageing process. Introduction In spite of being a biological phenomenon that has received much attention and given rise to numerous theories [1] , there are still many unanswered questions regarding the ageing process. Study species and holding condition The study was conducted using adult captive zebra finches Taeniopygia guttata , Vieillot. Data analysis Linear mixed-effects models with the identity of the bird included as a random effect were used to analyse the effect of age on BMR.

Results Basal metabolic rate controlled for the effect of body mass showed a significant decline with age in the zebra finches Table 1. Open in a separate window. Results from a mixed model with bird identity included as a random effect. Significance P is based on likelihood ratio test LR.

Figure 1. Figure 2. Figure 3. The effect of residual BMR on the hazard ratio for the risk of death for male A and female B zebra finches. Table 2 Result from a Cox proportional hazard survival analysis showing the effect of sex and BMR on survival of captive zebra finches. Discussion We found BMR to decline with age in a captive population of zebra finch. For instance, during short-term fasting phase, SIRT1 inhibits TORC2, a key mediator of early phase gluconeogenesis, leading to decreased gluconeogenesis SIRT1 also deacetylates and activates transcriptional factor Foxo1, resulting in increased gluconeogenesis A complete deletion of hepatic SIRT1 by floxing exons 5 and 6 leads to the development of liver steatosis even under normal chow diet Conversely, hepatic overexpression of SIRT1 mediated by adenovirus attenuates hepatic steatosis and ER stress, and restores glucose homeostasis in mice 48 , confirming the essential role of SIRT1 in maintaining hepatic metabolic homeostasis.

Recently, Kemper et al. Acetylation of FXR inhibits its activity and downregulation of hepatic SIRT1 increases FXR acetylation, causing deleterious metabolic outcomes such as liver steatosis and decreased bile output. Walker et al. In addition, chemical activators of SIRT1 inhibit SREBP target gene expression in vitro and in vivo , correlating with attenuated liver steatosis in diet-induced and genetically obese mice.

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In summary, these findings imply that hepatic SIRT1 plays a critical role in metabolic regulation and activation of SIRT1 in the liver may prove beneficial in treating obesity-associated diseases. The diverse functions of SIRT1 in central nutrient sensing and peripheral energy metabolism. The activity of SIRT1 is regulated by the cellular metabolic status, small molecule activators, interacting proteins, as well as post-translational modifications.

After activation, SIRT1 modulates a variety of metabolic activities systemically and locally through either direct protein deacetylation or indirect chromatin remodeling.


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Adipose tissue functions both to store fat and as a conduit for hormone signaling. For example, WAT-derived hormones such as leptin and adiponectin control energy balance, glucose regulation, and fatty acid catabolism. Consistently, treatment of mice on a high fat diet with resveratrol, a polyphenol that activates SIRT1, has been shown to protect against high-fat induced obesity and metabolic derangements 56 - Although the mechanisms of resveratrol's apparent protective effect on metabolic disorders are not fully understood, questions still remain whether or not resveratrol directly activates SIRT1 or functions through multiple signaling pathways 59 , 60 , these findings demonstrate that SIRT1 acts in concert with lipid regulating transcription factors to adapt gene transcription to changes in nutrient levels.

As an important non-shivering thermogenesis organ, brown adipose tissue BAT plays an essential role in survival of non-shivering animals and neonates. Dysfunction of these cells is the leading cause of type 1 diabetes mellitus, and partially contributes to the pathogenesis of type 2 diabetes. SIRT1 has been shown to be a major positive regulator for pancreatic insulin secretion, which in turn triggers glucose uptake and utilization.

In line with these observations, activation of SIRT1 by its activators in animals protects against high-fat induced obesity and insulin resistance 56 - 58 , and modest overexpression of SIRT1 has a protective effect against high-fat induced glucose intolerance 38 , These observations suggest that modulation of SIRT1 activity may regulate whole-body glucose metabolism at both systemically and locally.