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PubMedDate not supplied

Nutritional control of aging.

For more than 60 years the only dietary manipulation known to retard aging was caloric restriction, in which a variety of species respond to a reduction in energy intake by demonstrating extended median and maximum life span. More recently, two alternative dietary manipulations have been reported to also extend survival in rodents. Reducing the tryptophan content of the diet extends maximum life span, while lowering the content of sulfhydryl-containing amino acids in the diet by removing cysteine and restricting the concentration of methionine has been shown to extend all parameters of survival, and to maintain blood levels of the important anti-oxidant glutathione. To control for the possible reduction in energy intake in methionine-restricted rats, animals were offered the control diet in the quantity consumed by rats fed the low methionine diet. Such pair-fed animals experienced life span extension, indicating that methionine restriction-related life span extension is not a consequence of reduced energy intake. By feeding the methionine restricted diet to a variety of rat strains we determined that lowered methionine in the diet prolonged life in strains that have differing pathological profiles in aging, indicating that this intervention acts by altering the rate of aging, not by correcting some single defect in a single strain.

Aging↗

PubMed2004

Murine models of life span extension.

Mice are excellent experimental models for genetic research and are being used to investigate the genetic component of organismal aging. Several mutant mice are known to possess defects in the growth hormone/insulin-like growth factor 1 (GH/IGF-1) neurohormonal pathway and exhibit dwarfism together with extended life span. Their phenotypes resemble those of mice subjected to caloric restriction. Targeted mutations that affect components of this pathway, including the GH receptor, p66Shc, and the IGF-1 receptor (IGF-1R), also extend life span; mutations that affect IGF-1R or downstream components of the pathway decouple longevity effects from dwarfism. These effects on life span may result from an increased capacity to resist oxidative damage.

Aging↗

PubMed1993

Gallstone formation and weight loss.

Obesity is associated with increased bile stasis and cholesterol saturation, and an increased risk of gallstone development. Conversely, bile composition is normalized following reduction in body weight. It would appear advantageous to promote weight loss in obesity, which would reduce the predisposition to gallstone formation. Despite the potential health benefits of weight reduction, very-low-calorie diets appear to increase the risk for cholesterol crystal and gallstone formation. The incidence of gallstone formation seems to be dependent on the degree of caloric restriction, the rate of weight loss, and the duration of the dietary intervention. Thus, faster rates of weight loss for longer periods of time are associated with increased risk. Available data obtained from prospective studies of subjects during active weight loss suggest that newly formed gallstones occur within 4 weeks and with incidence rates 15 to 25-fold higher than in the general obese population. The stones produce symptoms in approximately one-third of the subjects, of whom approximately one-half will undergo surgery. Proposed mechanisms underlying gallstone formation during weight reduction include bile stasis due to reduced caloric intake, increased biliary cholesterol saturation secondary to increased cholesterol mobilization, and increased nucleation due to changes in bile arachidonate and glycoprotein concentrations. Data are lacking on the effects of gradual rates of weight loss and risk of gallstone formation.

Arachidonic Acids↗

PubMed2006

[Insulin resistance in pregnant type 1 diabetic female. Case report].

Insulin resistance may coexist with diabetes type 1 and make treatment of diabetes difficult. Case of 24-year-old type 1 diabetic female with insulin resistance features prior to pregnancy is reported. Exacerbating of insulin resistance during pregnancy was manifested by difficulties to overcome excessive weight gain and necessity to initiate treatment with high doses of insulin. The treatment was based on diet with progressive caloric restriction to 800 kcal/day in 35 week of pregnancy. That diet was continued till the delivery in 37 week. The fast acting analog insulin (Humalog) and long acting insulin (Humulin U) were used in treatment of diabetes. Treatment with low calorie diet did not cause negative effects on diabetic female metabolism and on the neonate state.

Adult↗

PubMed2006

Nutritional modulation of ageing: genomic and epigenetic approaches.

Dietary factors have a profound effect on many aspects of health including ageing and do so, at least partly, through interactions with the genome which result in altered gene expression. The application of high throughput genomics technologies in nutritional research (nutrigenomics) offers a new approach to understanding the molecular mechanisms by which nutrition affects ageing. To date, transcriptional profiling techniques have been applied in studies of the mode of action of energy (caloric) restriction. Two further areas which appear to be particularly promising are (i) nutritional modulation of DNA damage and repair and (ii) nutritional modulation of epigenetic markings. Epigenetic-mediated changes in gene expression in response to dietary and other lifestyle exposures appear to be a major molecular mechanism linking environmental factors with the genome with consequences for cell function and health throughout the life course.

Aged↗

PubMedDate not supplied

Birds as long-lived animal models for the study of aging.

Despite their high lifetime energy expenditures, most birds can be characterized as long-lived homeotherms with moderately slow aging. A growing body of research confirms the prediction that birds have special adaptations for preventing aging-related oxidative and glycoxidative damage. Nonetheless, biogerontologists have been slow to develop avian laboratory models. A number of domestic poultry and cage bird species represent either established or very promising animal models for studies of basic aging processes and their prevention, including degenerative neurobiological, behavioral and reproductive processes. Several kinds of birds have also been used in studies of cellular resistance to oxidative stressors in vitro. Results of preliminary studies on chickens and quail suggest that caloric restriction may extend the reproductive life span of hens, but its long-term effects on life span remain unstudied. Birds' innate anti-aging mechanisms may actually make them more suitable in some respects as models of longevity than short-lived laboratory rodents, and bird studies may ultimately reveal routes for therapeutic intervention in diseases of human aging and infertility.

Aging↗

PubMed2005

Gene expression profiling studies of aging in cardiac and skeletal muscles.

To examine transcriptional alterations associated with aging in skeletal muscle and the heart, we and others have used DNA microarrays to compare the gene expression profile of young and old animals. Aging results in a differential gene expression pattern specific to each tissue, and most alterations can be completely or partially prevented by caloric restriction (CR) in both heart and skeletal muscle. Transcriptional patterns of tissues from calorie-restricted animals suggests that CR retards the aging process by reducing endogenous damage and by inducing metabolic shifts associated with specific transcriptional profiles. These studies demonstrate that DNA microarrays can be used in cardiovascular aging research to generate panels of hundreds of transcriptional biomarkers, providing a new tool to measure biological age of cardiac and skeletal muscles and to test interventions designed to retard aging in these tissues.

Aging↗

PubMed2002

Role of oxidative stress and protein oxidation in the aging process.

The hypothesis is that the rate of oxygen consumption and the ensuing accrual of molecular oxidative damage constitute a fundamental mechanism governing the rate of aging is supported by several lines of evidence: (i) life spans of cold blooded animals and mammals with unstable basal metabolic rate (BMR) are extended and oxidative damage (OxD) is attenuated by an experimental decrease in metabolic rate; (ii) single gene mutations in Drosophila and Caenorhabditis elegans that extend life span almost invariably result in a generalized slowing of physiological activities, albeit via different mechanisms, affecting a decrease in OxD; (iii) caloric restriction decreases body temperature and OxD; and, (iv) results of studies on the effects of transgenic overexpressions of antioxidant enzymes are generally supportive, but quite ambiguous. It is suggested that oxidative damage to proteins plays a crucial role in aging because oxidized proteins lose catalytic function and are preferentially hydrolyzed. It is hypothesized that oxidative damage to specific proteins constitutes one of the mechanisms linking oxidative stress/damage and age-associated losses in physiological functions.

Aging↗

PubMed2005

[Eating and drinking during aging].

The retirement is a good moment in life to mirror one's health behaviour in regard to eating habits and physical activity. Based on the literature we recommend the Mediterranean "diet" in all ages. This diet is characterized by the intake of fresh fruit, vegetables, cereals, olive oil, fish, little meat, legumes, spices and herbs such as basil and garlic. A glass wine a day is legitimate. In increasing age total energy needs are decreasing. Therefore the energy intake has to be adjusted. Caloric restriction per se is a powerful means to reduce cardiovascular morbidity and mortality. However, not only the eating habits but also the entire lifestyle are important factors to influence cardiovascular mortality. Thus, the "low risk factors", i.e. Mediterranean diet, moderate alcohol consumption, physical activity and non-smoking must be controlled to improve health. In the HALE project the control of these factors reduced over-all mortality by 65 percent!

Aging↗

PubMed2006

The skinny on high-protein, low-carbohydrate diets.

Short-term studies of high-protein, low-carbohydrate diets have shown weight loss and improvements in plasma lipid profiles. Studies of greater than 6 months' duration, however, have failed to show continued benefit of high-protein, low-carbohydrate diets on weight loss and cardiovascular risk factors compared with conventional diets. Without concurrent weight loss and caloric restriction, these diets offer no additional benefit to lipids or body weight over other weight-loss regimens. In fact, high-protein, low-carbohydrate diets may add additional risk to individuals with cardiovascular disease due to their high fat and cholesterol content combined with decreased intake of fruits, vegetables, whole grains, and other nutrients related to cardiovascular risk. In addition, high-protein, low-carbohydrate diets have been implicated in other risks, including impaired renal, bone, and gastrointestinal health.

Caloric Restriction↗

PubMed2004

The role of macroautophagy in the ageing process, anti-ageing intervention and age-associated diseases.

Macroautophagy is a degradation/recycling system ubiquitous in eukariotic cells, which generates nutrients during fasting under the control of amino acids and hormones, and contributes to the turnover and rejuvenation of cellular components (long-lived proteins, cytomembranes and organelles). Tight coupling between these two functions may be the weak point in cell housekeeping. Ageing denotes a post-maturational deterioration of tissues and organs with the passage of time, due to the progressive accumulation of the misfunctioning cell components because of oxidative damage and an age-dependent decline of turnover rate and housekeeping. Caloric restriction (CR) and lower insulin levels may slow down many age-dependent processes and extend lifespan. Recent evidence is reviewed showing that autophagy is involved in ageing and in the anti-ageing action of anti-ageing calorie restriction: function of autophagy declines during adulthood and is almost negligible at older age; CR prevents the age-dependent decline of autophagic proteolysis and improves the sensitivity of liver cells to stimulation of lysosomal degradation; protection of autophagic proteolysis from the age-related decline co-varies with the duration and level of anti-ageing food restriction like the effects of CR extending lifespan; the pharmacological stimulation of macroautophagy has anti-ageing effects. Besides the involvement in ageing, macroautophagy may have an essential role in the pathogenesis of many age-associated diseases. Higher protein turnover may not fully account for the anti-ageing effects of macroautophagy, and effects of macroautophagy on housekeeping of the cell organelles, antioxidant machinery of cell membranes and transmembrane cell signaling should also be considered.

Aging↗

PubMed2005

Roles for leptin receptor/STAT3-dependent and -independent signals in the regulation of glucose homeostasis.

Leptin activates the long form of the leptin receptor (LRb) to control feeding and neuroendocrine function and thus regulate adiposity. While adiposity influences insulin sensitivity, leptin also regulates glucose homeostasis independently of energy balance. Disruption of the LRb/STAT3 signal in s/s mice results in hyperphagia, neuroendocrine dysfunction, and obesity similar to LRb null db/db mice. Insulin resistance and glucose intolerance are improved in s/s compared to db/db animals, however, suggesting that LRb/STAT3-independent signals may contribute to the regulation of glucose homeostasis by leptin. Indeed, caloric restriction normalized glycemic control in s/s animals, but db/db mice of similar weight and adiposity remained hyperglycemic. These differences in glucose homeostasis were not attributable to differences in insulin production between s/s and db/db animals but rather to decreased insulin resistance in s/s mice. Thus, in addition to LRb/STAT3-mediated adiposity signals, non-LRb/STAT3 leptin signals mediate an important adiposity-independent role in promoting glycemic control.

Amino Acid Substitution↗

PubMed1993

Enhancement of age-related increases in DNA I-compound levels by calorie restriction: comparison of male B-N and F-344 rats.

Caloric restriction (CR), known to extend median and maximum life spans, improve resistance to carcinogenesis, and significantly retard age-associated degenerative diseases in rodents, was previously reported to modulate levels of indigenous, age-dependent DNA modifications, called I-compounds, in male Brown-Norway (B-N) rats. Since profiles of these adduct-like derivatives are species-, strain-, sex-, and tissue-specific, we explored this apparent CR/I-compound relationship in a comparative study between male B-N and male Fischer 344 (F-344) rats, the latter having a shorter life expectancy and high incidence of renal disease. Control animals were fed NIH-31 diet ad libitum (AL), while the caloric intake of CR animals was limited to 60% of AL, starting at 3.5 months. Liver and kidney DNA from 1, 8, 12, 16, 24 (AL, CR), and 30 (CR only) month old rats was analyzed by 32P-postlabeling. Corresponding tissues from the two strains yielded similar DNA profiles. Total liver I-compound levels displayed 2.3-4.6-fold age-dependent increases from 1 to 24 months, and kidney values at 24 months were 5.2-8 times higher than those at 1 month. In both strains, I-compound levels of CR animals were higher, up to 2-fold, than in age-matched AL rats. Regression analyses indicated linear relationships between most CR relative adduct labeling values (both total and individual fractions) and age, whereas many AL values exhibited this type of link with log age. These findings confirm that a correlation exists between CR and I-compound levels, and, given the above physiological benefits of CR, indicate that I-compounds represent biomarkers of aging with potential utility in intervention studies.

Aging↗

PubMed2004

The genetics of human longevity.

Many of the genes that affect aging and longevity in model organisms, such as mice, fruit flies, and worms, have human homologs. This article reviews several genetic pathways that may extend lifespan through effects on aging, rather than through effects on diseases such as atherosclerosis or cancer. These include some of the genes involved in the regulation of DNA repair and nuclear structure, which cause the progeroid syndromes when mutated, as well as those that may affect telomere length, since shorter telomeres have been associated with shorter survival. Other potential longevity genes, such as sirtuins, are involved in regulating the response to cellular stress, including caloric restriction. The best-studied pathway involves insulin and insulin-like growth factor 1 signaling; mutations in homologs of these genes have extended lifespan up to sixfold in model organisms. Other potential candidates include mitochondrial DNA and the genes that regulate the inflammatory response. Despite the challenges in study design and analysis that face investigators in this area, the identification of genetic pathways that regulate longevity may suggest potential targets for therapy.

Aging↗

PubMed2004

Are we faced with two human species?

Problems could be found in the fact that we very often look for one deciding, definitive reason for the process of aging. It is a sort of search for a big discovery, like a fountain of youth or such. More and more authors are trying to explain the unknowns in the understanding of these observations about aging by adding the statement that there are two subgroups in the general population. This acknowledgment of two subpopulations explains why there are numerous cases that cannot be explained, defined, or fitted in basic observations about caloric restrictions and the delay of reproduction. The identification of those two groups would allow us to find more realistic results in studies and therefore a more efficient therapy of certain diseases. This hypothesis does not contradict theories of aging that we have accepted (at least not the majority of accepted theories), and this hypothesis also does not contradict the fact that there is a large interindividual variability. This hypothesis doubts, and claims there are exceptions to, the starting assumption of geriatrics and gerontology that: "parallel to the aging process the functions of all organs and organ systems lessen."

Aged↗

PubMed2003

Age-related changes of isoprenoid biosynthesis in rat liver and brain.

The physiological role of dolichol is not yet known but its accumulation in several tissues has been extensively reported in various physiological states or pathological conditions. Increased dolichol concentration in mammalian tissues during ageing has been also reported; in particular, we have previously indicated dolichol accumulation in liver as a new biomarker of ageing. However, the mechanism and the role of this accumulation is unknown. The aim of this work was to study the mechanism of the age-dependent dolichol accumulation analysing, in the liver and in the brain, the activity of the rate-limiting enzyme of isoprenoid biosynthesis, the 3-hydroxy 3-methylglutaryl CoA reductase, the dolichol and cholesterol synthesis on aged rats both fed ad libitum and caloric restricted. Furthermore, the dolichol and cholesterol levels in the plasma were assayed. The data shows that during ageing, the tissue dolichol accumulation is connected with the increase of 3-hydroxy 3-methylglutaryl CoA reductase activity and only in liver affected by diet restriction. In addition the aged rats maintain the capability to regulate their tissue cholesterol content by modifying cholesterol delivery into the blood. The amount of the 3-hydroxy 3-methylglutaryl CoA reductase enzyme detectable in liver and brain by Western blot analysis does not show significant changes during ageing. The presented data show that the accumulation of dolichol is related to the loss of enzymatic regulation characteristic of ageing. In fact, a higher mevalonate availability deriving from an increased expressed activity of HMGCoA-R could cause an increased production of dolichol.

Aging↗

PubMedDate not supplied

[Diet therapy of severe obesity].

In the last decades there has been a dramatic increase of obese subjects in many countries with the subsequent increase of health related problems, such as diabetes, hypertension, cardiovascular diseases. Even though several differential approaches, as media communication, guidelines formulation, have been performed in many different countries to solve this burden global health problem, no satisfactory results have been obtained. Personalized nutritional programs have been selected by obese subjects. Thus the correct approach would be to prescribe a caloric restricted diet in order to achieve long term weight loss in overweight or obese people. The aim in planning weight-reduction diets is that total food intake should meet recommended dietary allowance/adequate intake levels with the maintenance of the equilibrium among nutrients. If the nutritional approach fails or it is not sufficient to obtain significant weight loss, bariatric surgical intervention has been developed for the treatment of morbid-obese patients or severe obese patients with comorbidities as recommended by the American Society for Bariatric Surgery (A.S.B.S.) guidelines.

Bariatric Surgery↗

PubMed2005

The influence of dominant lethal mutations on litter size and body weight and the consequent impact on transgenerational carcinogenesis.

The reported untreated mouse control data from the Oak Ridge National Laboratory assessment of dominant damage (ADD) experiments demonstrate a strong negative correlation between body weight at 4, 5, 7, 9, and 11 weeks of age and number in litter at 3 weeks of age. Independently from the above finding, mother mice are also shown to differ substantially as to the mean weights of their litters. Much literature suggests that, as a general rule, (a) heavier mice are more likely to develop spontaneous and induced tumors earlier and (b) caloric restriction decreases body weights and tumor incidences and increases longevity. The above findings make it likely that many experiments that have been interpreted to demonstrate radiation-induced transgenerational carcinogenesis have instead merely illustrated a confounding effect of extensive induced dominant lethality. That is, because of induced dominant lethality, experimental groups contain heavier mice or rats, which accordingly develop more spontaneous tumors at a faster rate than control groups, with the increased tumor rates having nothing to do with induction of dominant tumor mutations. Our findings prompt suggestions as to possible modifications in the analysis and experimental design of such experiments.

Analysis of Variance↗