Carbohydrate metabolism in the elderly

Elahi, D; Müller, Dominik

doi:10.1038/sj.ejcn.1601032

Cited by 61 publications

(35 citation statements)

References 58 publications

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“…In clinical studies, both fasting glucose and hemoglobin A1c increase with aging even in the absence of diabetes (65). Thus, we postulated that the reduction of circulating glucose in the long-lived mice may reduce the frequency of glycations.…”

Section: Discussionmentioning

confidence: 99%

Low Utilization of Circulating Glucose after Food Withdrawal in Snell Dwarf Mice

Brooks

Trent

Raetzsch

et al. 2007

Journal of Biological Chemistry

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Glucose metabolism is altered in long-lived people and mice. Although it is clear that there is an association between altered glucose metabolism and longevity, it is not known whether this link is causal or not. Our current hypothesis is that decreased fasting glucose utilization may increase longevity by reducing oxygen radical production, a potential cause of aging. We observed that whole body fasting glucose utilization was lower in the Snell dwarf, a long-lived mutant mouse. Whole body fasting glucose utilization may be reduced by a decrease in the production of circulating glucose. Our isotope labeling analysis indicated both gluconeogenesis and glycogenolysis were suppressed in Snell dwarfs. Elevated circulating adiponectin may contribute to the reduction of glucose production in Snell dwarfs. Adiponectin lowered the appearance of glucose in the media over hepatoma cells by suppressing gluconeogenesis and glycogenolysis. The suppression of glucose production by adiponectin in vitro depended on AMP-activated protein kinase, a cell mediator of fatty acid oxidation. Elevated fatty acid oxidation was indicated in Snell dwarfs by increased utilization of circulating oleic acid, reduced intracellular triglyceride content, and increased phosphorylation of acetyl-CoA carboxylase. Finally, protein carbonyl content, a marker of oxygen radical damage, was decreased in Snell dwarfs. The correlation between high glucose utilization and elevated oxygen radical production was also observed in vitro by altering the concentrations of glucose and fatty acids in the media or pharmacologic inhibition of glucose and fatty acid oxidation with 4-hydroxycyanocinnamic acid and etomoxir, respectively.Glucose metabolism is altered in centenarians and long-lived mice (1-8). Our current hypothesis is that a decrease in fasting glucose utilization may increase longevity by lowering oxygen radical production, a potential cause of aging. Changes in glucose metabolism have been indicated in long-lived rodents by (a) oral glucose tolerance test, (b) insulin tolerance test, (c) inhibition of glucose production and stimulation of glucose disposal under euglycemic clamp conditions, and (d) the levels of circulating glucose and insulin under physiologic conditions (9 -13). These methods suggest that glucose utilization is elevated in long-lived mice during feeding. However, they do not reveal whether glucose utilization is lower in long-lived mice during fasting, a period of the day when glucose utilization is relatively low and fatty acid utilization is high.During fasting (a) the appearance in the circulation of glucose from the gastrointestinal tract is low, (b) the concentrations of circulating glucose and insulin are low, (c) circulating glucose is used for energy rather than storage, and (d) the circulating glucose used is replenished largely by liver glucose production, via gluconeogenesis and glycogenolysis. Thus, whole body glucose utilization may be lowered during fasting by decreasing glucose production. Whether fasting glucose pro...

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Section: Discussionmentioning

confidence: 99%

Low Utilization of Circulating Glucose after Food Withdrawal in Snell Dwarf Mice

Brooks

Trent

Raetzsch

et al. 2007

Journal of Biological Chemistry

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“…Specifically, CR blunts sexual maturation and fertility, which allows longterm survival through energy sparing, 22 and reverses aginginduced reduction in insulin resistance. [23][24][25][26] Reproductive function and insulin resistance are both closely related to body fat mass and are both affected by hormones produced by adipocytes. 27 Besides these, free fatty acids (FFA), released in the circulation as a result of lipolysis in WAT, also strongly induce insulin resistance when they are not promptly oxidized in other tissues.…”

Section: Introductionmentioning

confidence: 99%

Molecular links between aging and adipose tissue

Picard

Guarente

2005

Int J Obes

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White adipose tissue now emerges as a pivotal organ controlling lifespan. Calorie restriction, which so far extends lifespan in all organisms, primarily affects energy stores in adipose tissue. Genetic manipulations aiming at modifying fat mass also impact on the duration of life in several model organisms. We recently proposed that silent information regulator 2 (SIR2) ortholog, sirtuin 1 (SIRT1), the mammalian ortholog of the life-extending yeast gene SIR2, is involved in the molecular mechanisms linking lifespan to adipose tissue. SIRT1 represses peroxisome proliferator-activated receptors gamma transactivation and inhibits lipid accumulation in adipocytes. The effect of adipose tissue reduction on lifespan could be due to the production of adipokines acting on target tissues such as the brain, or due to the indirect prevention of age-related metabolic disorders like type 2 diabetes or atherosclerosis.

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“…This syndrome mainly arises from muscle metabolic dysfunction and changes in body composition [31,32]. These dysfunctions and shifts are accompanied by a decreased metabolic function of the whole metabolism (especially mitochondria) leading to reduced overall activity [33].…”

Section: Carbohydrate Metabolismmentioning

confidence: 99%

Overview of the physiological changes and optimal diet in the golden age generation over 50

Gille

2010

Eur Rev Aging Phys Act

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Basically, our lifespan is determined genetically. However, several other parameters such as the environment, lifestyle and diet have a high impact on living in the best of health. Many older persons suffer from various diseases, which often cannot be avoided; however, their development can be postponed and symptoms can be mitigated by a balanced diet, moderate physical activity as well as a healthy lifestyle. These diseases are, for example, sarcopenia (degenerative loss of muscle mass), osteoporosis (decomposition of bone structure), digestive restrictions, sensory impairment, water imbalance or a compromised immune system. Psychological modifications, obesity and loss of weight also commonly occur in older adults. To define an adequate diet for elderly between the ages 50 and 80 is difficult, even impossible, because the nutritional requirements differ between the dynamic quinquagenarian and the frailer eighty-year-old. However, several studies have shown that sufficient consumption of high-quality proteins, calcium, vitamin D, anti-oxidative food compounds, water as well as adapted energy values and nourishment with high-nutrient density in combination with physical activity especially help one to remain healthy to a great age. The cornerstone of healthy ageing is the maintenance of normal bodyweight in order to prevent the development of diseases such as osteoporosis, coronary heart disease or diabetes type 2. This publication will review the physiological changes that occur with advanced age and consequential nutritional recommendations for elderly persons.

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Carbohydrate metabolism in the elderly

Cited by 61 publications

References 58 publications

Low Utilization of Circulating Glucose after Food Withdrawal in Snell Dwarf Mice

Low Utilization of Circulating Glucose after Food Withdrawal in Snell Dwarf Mice

Molecular links between aging and adipose tissue

Overview of the physiological changes and optimal diet in the golden age generation over 50

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