Do Ames dwarf and calorie-restricted mice share common effects on age-related pathology?

نویسندگان

  • Yuji Ikeno
  • Gene B. Hubbard
  • Shuko Lee
  • Sara M. Dube
  • Lisa C. Flores
  • Madeline G. Roman
  • Andrzej Bartke
چکیده

Since 1996, aging studies using several strains of long-lived mutant mice have been conducted. Among these studies, Ames dwarf mice have been extensively examined to seek clues regarding the role of the growth hormone/insulin-like growth factor-1 axis in the aging process. Interestingly, these projects demonstrate that Ames dwarf mice have physiological characteristics that are similar to those seen with calorie restriction, which has been the most effective experimental manipulation capable of extending lifespan in various species. However, this introduces the question of whether Ames dwarf and calorie-restricted (CR) mice have an extended lifespan through common or independent pathways. To answer this question, we compared the disease profiles of Ames dwarf mice to their normal siblings fed either ad libitum (AL) or a CR diet. Our findings show that the changes in age-related diseases between AL-fed Ames dwarf mice and CR wild-type siblings were similar but not identical. Moreover, the effects of CR on age-related pathology showed similarities and differences between Ames dwarf mice and their normal siblings, indicating that calorie restriction and Ames dwarf mice exhibit their anti-aging effects through both independent and common mechanisms.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

The effect of calorie restriction on insulin signaling in skeletal muscle and adipose tissue of Ames dwarf mice

Long-living Ames dwarf (df/df) mice are homozygous for a mutation of the Prop1(df) gene. As a result, mice are deficient in growth hormone (GH), prolactin (PRL) and thyrotropin (TSH). In spite of the hormonal deficiencies, df/df mice live significantly longer and healthier lives compared to their wild type siblings. We studied the effects of calorie restriction (CR) on the expression of insulin...

متن کامل

How diet interacts with longevity genes

In laboratory mice, suppression of growth hormone (GH) signaling by spontaneous mutations or targeted disruption of GHor IGF1-related genes can lead to an impressive increase of longevity. Hypopituitary Ames dwarf (Prop1) and GH receptor knockout (GHRKO) mice live 35-70% longer than their normal littermates. Many phenotypic characteristics of these longlived mutants resemble findings in genetic...

متن کامل

Metabolic characteristics of long-lived mice

Genetic suppression of insulin/insulin-like growth factor signaling (IIS) can extend longevity in worms, insects, and mammals. In laboratory mice, mutations with the greatest, most consistent, and best documented positive impact on lifespan are those that disrupt growth hormone (GH) release or actions. These mutations lead to major alterations in IIS but also have a variety of effects that are ...

متن کامل

Circulating microRNA signature of genotype‐by‐age interactions in the long‐lived Ames dwarf mouse

Recent evidence demonstrates that serum levels of specific miRNAs significantly change with age. The ability of circulating sncRNAs to act as signaling molecules and regulate a broad spectrum of cellular functions implicates them as key players in the aging process. To discover circulating sncRNAs that impact aging in the long-lived Ames dwarf mice, we conducted deep sequencing of small RNAs ex...

متن کامل

Divergent effects of caloric restriction on gene expression in normal and long-lived mice.

Long-lived Ames dwarf mice share many phenotypic characteristics with animals subjected to caloric restriction (CR) but they are not CR mimetics. CR prolongs longevity in both normal and Ames dwarf mice. Using real-time polymerase chain reaction and western blot, we have examined the expression of genes related to insulin signaling in the liver of normal and dwarf mice subjected to 30% CR. The ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 3  شماره 

صفحات  -

تاریخ انتشار 2013