Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage

Many previous investigations have consistently reported that caloric restriction (40%), which increases maximum longevity, decreases mitochondrial reactive species (ROS) generation and oxidative damage to mitochondrial DNA (mtDNA) in laboratory rodents. These decreases take place in rat liver after only seven weeks of caloric restriction. Moreover, it has been found that seven weeks of 40% protein restriction, independently of caloric restriction, also decrease these two parameters, whereas they are not changed after seven weeks of 40% lipid restriction. This is interesting since it is known that protein restriction can extend longevity in rodents, whereas lipid restriction does not have such effect. However, before concluding that the ameliorating effects of caloric restriction on mitochondrial oxidative stress are due to restriction in protein intake, studies on the third energetic component of the diet, carbohydrates, are needed. In the present study, using semipurified diets, the carbohydrate ingestion of male Wistar rats was decreased by 40% below controls without changing the level of intake of the other dietary components. After seven weeks of treatment the liver mitochondria of the carbohydrate restricted animals did not show changes in the rate of mitochondrial ROS production, mitochondrial oxygen consumption or percent free radical leak with any substrate (complex I- or complex II-linked) studied. In agreement with this, the levels of oxidative damage in hepatic mtDNA and nuclear DNA were not modified in carbohydrate restricted animals. Oxidative damage in mtDNA was one order of magnitude higher than that in nuclear DNA in both dietary groups. These results, together with previous ones, discard lipids and carbohydrates, and indicate that the lowered ingestion of dietary proteins is responsible for the decrease in mitochondrial ROS production and oxidative damage in mtDNA that occurs during caloric restriction.     

Dietary polyunsaturated fatty acids and heme iron induce oxidative stress biomarkers and a cancer promoting environment in the colon of rats

The end products of polyunsaturated fatty acid (PUFA) peroxidation, such as malondialdehyde (MDA), 4-hydroxynonenal (HNE), and isoprostanes (8-iso-PGF_2α), are widely used as systemic lipid oxidation/oxidative stress biomarkers. However, some of these compounds have also a dietary origin. Thus, replacing dietary saturated fat by PUFAs would improve health but could also increase the formation of such compounds, especially in the case of a pro-oxidant/antioxidant imbalanced diet. Hence, the possible impact of dietary fatty acids and pro-oxidant compounds was studied in rats given diets allowing comparison of the effects of heme iron vs. ferric citrate and of ω-6- vs. ω-3-rich oil on the level of lipid peroxidation/oxidative stress biomarkers. Rats given a heme iron-rich diet without PUFA were used as controls. The results obtained have shown that MDA and the major urinary metabolite of HNE (the mercapturic acid of dihydroxynonane, DHN-MA) were highly dependent on the dietary factors tested, while 8-iso-PGF_2α was modestly but significantly affected. Intestinal inflammation and tissue fatty acid composition were checked in parallel and could only explain the differences we observed to a limited extent. Thus, the differences in biomarkers were attributed to the formation of lipid oxidation compounds in food or during digestion, their intestinal absorption, and their excretion into urine. Moreover, fecal extracts from the rats fed the heme iron or fish oil diets were highly toxic for immortalized mouse colon cells. Such toxicity can eventually lead to promotion of colorectal carcinogenesis, supporting the epidemiological findings between red meat intake and colorectal cancer risk.Therefore, the analysis of these biomarkers of lipid peroxidation/oxidative stress in urine should be used with caution when dietary factors are not well controlled, while control of their possible dietary intake is needed also because of their pro-inflammatory, toxic, and even cocarcinogenic effects.     

Randomized controlled trial of dietary intervention: association between level of urinary phenolics and anti-mutagenicity

We have undertaken a randomized trial to confirm the ability of a class of phenolics, flavonoids, to increase urinary anti-mutagenicity in smokers. Ninety heavy smokers were recruited and randomly assigned to three groups, who were given three different diets. One diet was rich in flavonoids, but not based on supplementation ('flavonoid'), one was a normal iso-caloric diet with an adequate administration of fruit and vegetables ('normal'), and one was based on supplementation of flavonoids in the form of green tea and soy products ('supplement'). The urinary anti-mutagenicity-as inhibiting effect of the urinary extracts on the mutations induced by MeIQx-was measured in Salmonella typhimurium YG1024 in the presence of liver S9 from male Sprague-Dawley rats treated with Aroclor 1254. The amount of total phenolics in the urinary extracts was measured by use of spectrometric analysis. We found that important dietary modifications can be achieved through special recipes and instructions given by a cook during an intensive course. The intervention was focused on increasing the flavonoid intake, and it was successful in that respect. In fact, differences in flavonoid intake were appreciated mainly between the first group (normal diet) and the other two (flavonoid-rich and supplemented diet), suggesting that dietary modification can be as effective as supplementation. However, both urinary anti-mutagenicity and the amounts of urinary phenolics did not change as a consequence of the trial. These results suggest that only a small fraction of urinary phenolics is influenced by dietary changes in the intake of flavonoids, and that most urinary anti-mutagens and phenolics are metabolites of dietary flavonoids, whose formation is more affected by the activity and diversity of bacterial flora in the colon than by the quantity and type of intake. A strong correlation was found between urinary phenolics and anti-mutagenicity in all the groups involved in the trial. Such correlation was not explained by dietary variables.     

Protein Restriction Without Strong Caloric Restriction Decreases Mitochondrial Oxygen Radical Production and Oxidative DNA Damage in Rat Liver

Previous studies have shown that caloric restriction decreases mitochondrial oxygen radical production and oxidative DNA damage in rat organs, which can be linked to the slowing of aging rate induced by this regime. These two characteristics are also typical of long-lived animals. However, it has never been investigated if those decreases are linked to the decrease in the intake of calories themselves or to decreases in specific dietary components. In this study the possible role of the dietary protein was investigated. Using semipurified diets, the ingestion of proteins of Wistar rats was decreased by 40% below that of controls while the other dietary components were ingested at the same level as in animals fed ad libitum. After seven weeks in this regime the liver of the protein restricted animals showed 30–40% decreases in mitochondrial production of reactive oxygen species (ROS) and in oxidative damage to nuclear and mitochondrial DNA. The decreases in ROS generation occurred specifically at complex~I. They also occurred without changes in mitochondrial oxygen consumption. Instead, there was a decrease in the percent free radical leak (the percentage of total electron flow leading to ROS generation in the respiratory chain). These results are strikingly similar to those previously obtained after 40% caloric restriction in the liver of Wistar rats. Thus, the results suggest that part of the decrease in aging rate induced by caloric restriction can be due to the decreased intake of proteins acting through decreases in mitochondrial ROS production and oxidative DNA damage. Interestingly, these tissue oxidative stress-linked parameters can be lowered by restricting only the intake of dietary protein, probably a more feasible option than caloric restriction for adult humans.     

Nutritional composition of the diet of the western gorilla (Gorilla gorilla): Interspecific variation in diet quality

To meet nutritional needs, primates adjust their diets in response to local habitat differences, though whether these dietary modifications translate to changes in dietary nutrient intake is unknown. A previous study of two populations of the mountain gorilla (MG: Gorilla beringei) found no evidence for intraspecific variation in the nutrient composition of their diets, despite ecological and dietary differences between sites. One potential explanation is that nutritional variability in primate diets requires greater ecological divergence than what was captured between MG sites, underpinning environmental differences in the nutrient quality of plant foods. To test whether Gorilla exhibits interspecific variation in dietary composition and nutrient intake, we studied the composition and macronutrients of the western gorilla (WG: Gorilla gorilla) staple diets and compared them with published data from the two MG populations. We recorded feeding time and food intake of four adult female WGs from one habituated group over a period of 11 months (December 2004–October 2005) at the Mondika Research Center, Republic of Congo, allowing for assessment of seasonal patterns of nutrient intake. Staple diets of WGs and MGs diverged in their dietary and macronutrient composition. Compared to MGs, the staple diet of WGs (by intake) contained higher proportions of fruit (43%) and leaf (12%) and a lower proportion of herb (39%), resulting in a higher intake of total nonstructural carbohydrate and fiber and a lower intake of crude protein. Staple gorilla fruits and herbs differed in nutrient quality between sites. Gorillas exhibit nutritional flexibility that reflects ecological variation in the nutrient quality of plant foods. Since dietary quality typically affects rates of growth and reproduction in primates, our results suggest that interspecific differences in nutrient intake and food quality may shape differences in gorilla nutrient balancing and female life history strategies.     

Dietary Silicon Intake of Korean Young Adult Males and Its Relation to their Bone Status

Accumulated data suggests a positive effect of silicon on bone health; however, limited research exists on the silicon content of foods. To further the understanding of the relationship between dietary silicon intake and bone health, a food composition database of commonly consumed foods in Korea is required. For quantitative data on the intake levels of silicon, we analyzed the silicon content of 365 food items commonly consumed in Korea using inductively coupled plasma—atomic emission spectrometry following microwave-assisted digestion. To investigate the dietary silicon intake status and to examine the potential role of dietary silicon intake in the bone status of men, a total of 400 healthy Korean adult males aged 19–25 were observed for their diet intake and calcaneus bone density using the 24-h recall method and quantitative ultrasound, respectively. Clinical markers reflecting bone metabolism such as serum total alkaline phosphatase, N-mid osteocalcin, and type 1 collagen C-terminal telopeptide concentrations were also analyzed. Silicon intake of the subjects was estimated as 37.5 ± 22.2 mg/day. Major food sources of dietary silicon in the Korean male were cereal and cereal products (25.6 % of total silicon intake), vegetables (22.7 %), beverages and liquors (21.2 %), and milk and milk products (7.0 %). Silicon intake correlated positively with age, weight, energy intake, protein intake, calcium intake, and alcohol intake. After adjusted for age, weight, energy intake, protein intake, calcium intake, alcohol intake, smoking cigarettes, and regular exercise status, daily total silicon intake had no correlation with calcaneus bone density and the bone metabolism markers, but silicon intake from vegetables had a positive correlation with serum total alkaline phosphatase activity, a bone formation maker. These findings show the possible positive relationship between dietary silicon intake from vegetables and the bone formation of young adult males. Further investigation in a larger (Korean) population and correcting for additional nutritional confounders is required to confirm these findings.     

Dietary fat increases energy intake across the range of typical consumption in the United States

Objective: The fat content of a diet has been shown to affect total energy intake, but controlled feeding trials have only compared very high (40% of total calories) fat diets with very low (20% of total calories) fat diets. This study was designed to measure accurately the voluntary food and energy intake over a range of typical intake for dietary fat. Methods and Procedures: Twenty‐two non‐obese subjects were studied for 4 days on each of three diets, which included core foods designed to contain 26, 34, and 40% fat, respectively of total calories and ad lib buffet foods of similar fat content. All diets were matched for determinants of energy density except dietary fat. Subjects consumed two meals/day in an inpatient unit and were provided the third meal and snack foods while on each diet. All food provided and not eaten was measured by research staff. Results: Voluntary energy intake increased significantly as dietary fat content increased (P = 0.008). On the 26% dietary fat treatment, subjects consumed 23.8% dietary fat (core and ad lib foods combined) and 2,748 ± 741 kcal/day (mean ± s.d.); at 34% dietary fat, subjects consumed 32.7% fat and 2,983 ± 886 kcal/day; and at 40% dietary fat subjects consumed 38.1% fat and 3,018 ± 963 kcal/day. Discussion: These results show that energy intake increases as dietary fat content increases across the usual range of dietary fat consumed in the United States. Even small reductions in dietary fat could help in lowering total energy intake and reducing weight gain in the population.     

Assessment of dietary exposure related to dietary GI and fibre intake in a nutritional metabolomic study of human urine

There is a need for a tool to assess dietary intake related to the habitual dietary glycaemic index (GI) and fibre in groups with large numbers of individuals. Novel metabolite-profiling techniques may be a useful approach when applied to human urine. In a long-term, controlled dietary intervention study, metabolomics were applied to assess dietary patterns. A targeted approach was used to evaluate the effects on urinary C-peptide excretion caused by the dietary treatments. Seventy-seven overweight subjects followed an 8-week low-calorie diet (LCD) and were then randomly assigned to a high-GI or low-GI diet for 6 month during which they completed 24-h urine collections at baseline (prior to the 8-week LCD) and after randomisation to the dietary intervention, at month 1, 3 and 6, respectively. Metabolite profiling in 24-h urine was performed by ¹H NMR and chemometrics. Partial least squares (PLS) analysis indicated that urinary formate could discriminate between high-GI and low-GI diets (correlation coefficient r = 0.82), and this finding was confirmed statistically (P = 0.01). PLS analysis also indicated that urinary hippurate could be associated with fibre intake, but this finding was not confirmed statistically. No associations between GI and urinary C-peptide were found. Our results emphasise that application of metabolomics is useful in the assessment of dietary exposure related to dietary GI and fibre seen at group level in a nutritional metabolomic study of human urine. As our design allowed for large variations in individually selected food items, biomarkers identified at group level may be interpreted as more general and robust markers, largely not confounded with markers from single dietary factors.     

Conserved and differential effects of dietary energy intake on the hippocampal transcriptomes of females and males

The level of dietary energy intake influences metabolism, reproductive function, the development of age-related diseases, and even cognitive behavior. Because males and females typically play different roles in the acquisition and allocation of energy resources, we reasoned that dietary energy intake might differentially affect the brains of males and females at the molecular level. To test this hypothesis, we performed a gene array analysis of the hippocampus in male and female rats that had been maintained for 6 months on either ad libitum (control), 20% caloric restriction (CR), 40% CR, intermittent fasting (IF) or high fat/high glucose (HFG) diets. These diets resulted in expected changes in body weight, and circulating levels of glucose, insulin and leptin. However, the CR diets significantly increased the size of the hippocampus of females, but not males. Multiple genes were regulated coherently in response to energy restriction diets in females, but not in males. Functional physiological pathway analyses showed that the 20% CR diet down-regulated genes involved in glycolysis and mitochondrial ATP production in males, whereas these metabolic pathways were up-regulated in females. The 40% CR diet up-regulated genes involved in glycolysis, protein deacetylation, PGC-1alpha and mTor pathways in both sexes. IF down-regulated many genes in males including those involved in protein degradation and apoptosis, but up-regulated many genes in females including those involved in cellular energy metabolism, cell cycle regulation and protein deacetylation. Genes involved in energy metabolism, oxidative stress responses and cell death were affected by the HFG diet in both males and females. The gender-specific molecular genetic responses of hippocampal cells to variations in dietary energy intake identified in this study may mediate differential behavioral responses of males and females to differences in energy availability.     

Bioavailability of selenium from meat and broccoli as determined by retention and distribution of 75Se

The concentration of selenium (Se), an essential nutrient, is variable in foods, depending, in part, on how and where foods are produced; some foods accumulate substantial amounts of Se when produced on high-Se soils. The chemical form of Se also differs among foods. Broccoli is a Se-accumulating plant that contains many methylated forms of Se, and Se bioavailability from broccoli has been reported to be low. Red meats such as pork or beef could accumulate Se when the animal is fed high-Se diets, and Se from such meats has been reported to be highly bioavailable for selenoprotein synthesis. In a further attempt to characterize the utilization of Se from broccoli and meats such as pork or beef, we have fed rats diets adequate (0.1 μg Se/g diet) in Se or high in Se (1.5 μg S/g diet), with the Se source being either high-Se broccoli or beef. Rats were then given test meals of broccoli or pork intrinsically labeled with ⁷⁵Se. When dietary Se was nutritionally adequate (0.1 μg/g diet), more ⁷⁵Se from pork than broccoli was retained in tissues; however, there were no significant differences in whole-body retention when dietary Se was high (1.5 μg/g diet). A significantly greater percentage of ⁷⁵Se from broccoli than pork was excreted in the urine and dietary Se did not affect urinary excretion of broccoli ⁷⁵Se, but the amount excreted from pork varied directly with dietary Se intake. Radiolabeled ⁷⁵Se derived from pork effectively labeled selenoproteins in all tissues examined, but ⁷⁵Se from broccoli was undetectable in selenoproteins. These differences in retention and distribution of Se from broccoli or pork are consistent with reported differences in bioavailability of Se from beef and broccoli. They also suggest that there are fewer differences in bioavailability when Se is consumed in supranutritional amounts.     

Hepatic and adipose tissue lipogenic enzyme mRNA levels are suppressed by high fat diets in the rat

Small changes in lipogenic enzyme activity induced by dietary fats of different composition may, over the long term, have significant impact on the development of obesity. We have investigated the effect of high fat diets (45% of calories as fat) on abundance of mRNA encoding fatty acid synthetase (FAS) and glycerophosphate dehydrogenase (GPDH) in male Sprague-Dawley rats. When caloric intake was equal, the relative amount of hepatic FAS mRNA was greater in rats fed a saturated compared to a polyunsaturated fat diet. This difference could not be attributed to diet-induced changes in plasma insulin concentration. However, both fat diets suppressed hepatic FAS mRNA compared to a sucrose diet. Close correlation between FAS specific activity and the relative amount of mRNA suggested that regulation was mainly at a pre-translational level. Adipose tissue FAS mRNA was suppressed by the two fat diets equally while GPDH mRNA was unaffected by dietary composition. Retroperitoneal fat pads were significantly larger in rats fed saturated compared to those fed polyunsaturated fat for 26 weeks. We concluded that dietary saturated fats fail to suppress hepatic de novo lipogenesis as effectively as polyunsaturated fats, which may have implications for the prevention of obesity in humans.     

The influence of dietary flaxseed and other grains, fruits and vegetables on the frequency of spontaneous chromosomal damage in mice

Spontaneous genetic damage, whether mutations or chromosomal aberrations, undoubtedly arise from a variety of sources including replication errors, oxidative damage, background radiation, and chemical exposure. Given the numerous correlations between diet and cancer, it seemed possible that diet could influence the spontaneous rate of DNA damage and its genetic consequences. Since diets high in vegetables, fruits, and grains are associated with lower rates of cancer, we supplemented the diets of mice and measured the frequency of micronuclei in the peripheral blood. Micronuclei arise from broken chromosomes or chromosome loss in the erythroblast. They are first seen in the short reticulocyte stage of the red blood cell but persist for the entire 30-day lifespan of the cell in mice. C57Bl mice were placed on a defined diet (AIN-93G) supplemented to 20% final dry weight with grains or freeze-dried fruits or vegetables. The micronucleus frequency was measured in a pre-exposure blood sample and every 2 weeks thereafter for 6 weeks. This was possible in spite of the low spontaneous frequency of 1/1000-2/1000 cells by the use of a novel flow cytometric method, which permitted the analysis of both the mature red blood cells and reticulocytes. Of the foods tested, flaxseed proved to be the most protective by reducing the incidence of micronuclei in both the reticulocyte and normochromatic erythrocyte cell populations by 30 and 11%, respectively. The results show that at least one class of spontaneous genetic damage can be modified by diet and suggests that short-term experiments with small numbers of animals can be used to identify dietary anticarcinogens that may influence human cancer rates.     

Effects of diet on biomarkers of exposure and effects, and on oxidative damage

Modification of DNA is believed to be a key step in carcinogenesis, and therefore DNA adducts have been proposed as predictive biomarkers of human cancer. Smoked and grilled foods are important contributors of PAH-DNA adduct levels, while the consumption of flavonoids and other antioxidants seems to decrease the level of DNA adducts. The aim of this study was to assess the effect of each group of foods and of different dietary profiles on the DNA adducts levels and on oxidative damage to DNA. Occupationally exposed men were recruited in Czech Republic, Slovak Republic and Bulgaria. Non-occupationally exposed subjects were matched on age and gender to PAH-exposed workers. Three hundred and fifty-six subjects who completed the questionnaire for dietary information and had a measurement of DNA adduct levels and oxidative damage to DNA were included in this study. No food item seemed to be individually associated with markers of exposure or DNA damage. Total DNA adducts levels were significantly higher for subjects who had eaten, in the previous 24 h, smoked or fried food. A Principal Components Analysis was performed to identify groups of subjects with similar dietary profiles: no significant differences in biomarker levels were observed among the groups defined according to dietary profiles. In conclusion, this study did not show any significant association between diet and biomarkers of DNA damage, oxidative damage to DNA and chromosomal aberrations, neither when each food was considered separately, nor when the effect of different dietary profiles was tested. The recent consumption of smoked or fried food was associated with an increase in total DNA adducts levels.     

Adipose tissue and the effects of fat and calories on breast tumorigenesis in rats

A high fat diet fed ad libitum will promote breast tumorigenesis in rats while caloric restriction of the same high fat diet counteracts this promotional effect. The present study examined the effects of dietary fat and calorie intake on adipose tissue weight and fatty acid composition and on tumor incidence and development. The sites of adipose tissue chosen were the mammary fat pad, representing adipose tissue in the immediate location of the studied tumor, and the abdominal fat depot which in humans has been associated with an increased risk of breast cancer. High (20% corn oil) and low (5% corn oil) fat test diets were offered ad libitum and at 40% restriction levels. In agreement with prior studies, caloric restriction of both high and low fat diets led to marked decreases in tumor incidence (63 to 68% versus 21%), tumor burden (1.84 to 2.05 versus 0.37 to 0.43 tumors/rat), and tumor weight (7.1 to 11.9 versus 1.4 to 2.2 g) at the time of sacrifice (133 days post-DMBA). While final body weights were reduced in proportion to the level of caloric restriction (290 to 291 g versus 184 to 201 g), abdominal fat (8.8 to 9.2 versus 0.9 to 1.6 g), and mammary fat weights (3.1 to 4.1 versus 0.7 to 2.0 g) were reduced markedly in association with the decrease in tumorigenesis. While both tumor and mammary fat were enriched with linoleate reflecting the fatty acid composition of dietary fat, the ratio of arachidonic acid to linoleic acid was higher in tumor tissue than in surrounding normal mammary tissue in both the phospholipid (0.78 versus 0.18) and neutral lipid fractions (0.22 versus 0.03). These observations are consistent with the concept that increases in fat tissue mass in abdominal and mammary fat depots may mediate some of the promotional effects of high fat and high calorie diets. Restriction of dietary fat and calories to reduce body fat and strategies to modify the composition of stored lipids in fat depots may offer nutritional approaches to breast cancer prevention and treatment.     

Dietary Fat Dose Dependently Increases Spontaneous Caloric Intake in Rat

Objective: To characterize the dose‐response relationship between dietary fat to carbohydrate ratio and spontaneous caloric intake. Research Methods and Procedures: Male Long‐Evans rats consumed milk‐based liquid diets that differed in fat content (17% to 60% of kilocalories) but had equivalent protein content and energy density. In Experiment 1, rats consumed one of the diets (n = 9/diet group) as the sole source of nutrition for 16 days. In Experiment 2, diets were offered as an option to nutritionally complete chow for 4 days followed by a 3‐day chow‐only washout in a randomized within‐subjects design (n = 30). In Experiment 3, nine rats received isocaloric intragastric infusions of diet overnight, with chow available ad libitum. At least two no‐infusion days separated the different diet infusions, which were given in random order. Food intake was measured daily Results: Dietary fat dose dependently increased total daily kilocalories in each of the three paradigms. Discussion: These data imply that the postingestive effects of carbohydrate and fat differentially engage the physiological substrates that regulate daily caloric intake. These findings reiterate the importance of investigating macronutrient‐specific controls of feeding, rather than prematurely concluding that dietary attributes that covary with fat content (e.g., caloric density and palatability) drive the overeating associated with a high‐fat diet.     

Urinary biomarkers and the rate of DNA damage in carcinogenesis and anticarcinogenesis.

Endogenous oxidative processes are shown to generate hydrogen peroxide and .OH radicals, which react in vivo to form a variety of products. Thymidine glycol (Tg) and 8-hydroxydeoxyguanosine (8-dRG-OH) are such products. They result from the excision repair of DNA and are excreted in urine. Both products can be used as biomarkers in the dosimetry of oxidative damage to DNA. Since oxidative processes and accumulation of their effects contribute to carcinogenesis, the proposed rate-of-damage hypothesis provides a rationale for using these biomarkers in early diagnostics and in the assessment of carcinogenic and anticarcinogenic properties of diets, foods, and food components, as well as certain exogenous toxicants and agents. Approaches for measurement of urinary biomarkers of DNA damage are reviewed.     

Fatty acid composition of adipose tissue and blood in humans and its use as a biomarker of dietary intake

Accurate assessment of fat intake is essential to examine the relationships between diet and disease risk but the process of estimating individual intakes of fat quality by dietary assessment is difficult. Tissue and blood fatty acids, because they are mainly derived from the diet, have been used as biomarkers of dietary intake for a number of years. We review evidence from a wide variety of cross-sectional and intervention studies and summarise typical values for fatty acid composition in adipose tissue and blood lipids and changes that can be expected in response to varying dietary intake. Studies in which dietary intake was strictly controlled confirm that fatty acid biomarkers can complement dietary assessment methodologies and have the potential to be used more quantitatively. Factors affecting adipose tissue and blood lipid composition are discussed, such as the physical properties of triacylglycerol, total dietary fat intake and endogenous fatty acid synthesis. The relationship between plasma lipoprotein concentrations and total plasma fatty acid composition, and the use of fatty acid ratios as indices of enzyme activity are also addressed.     

Dietary composition specifies consumption, obesity, and lifespan in Drosophila melanogaster

The inability to properly balance energy intake and expenditure with nutrient supply forms the basis for some of today's most pressing health issues, including diabetes and obesity. Mechanisms of nutrient homeostasis may also lie at the root of dietary restriction, a manipulation whereby reduced nutrient availability extends lifespan and ameliorates age-related deteriorations in many species. The traditional belief that the most important aspect of the diet is its energetic (i.e. caloric) content is currently under scrutiny. Hypotheses that focus on diet composition and highlight more subtle characteristics are beginning to emerge. Using Drosophila melanogaster , we asked whether diet composition alone, independent of its caloric content, was sufficient to impact behavior, physiology, and lifespan. We found that providing flies with a yeast-rich diet produced lean, reproductively competent animals with reduced feeding rates. Excess dietary sugar, on the other hand, promoted obesity, which was magnified during aging. Addition of dietary yeast often limited or reversed the phenotypic changes associated with increased dietary sugar and vice versa, and dietary imbalance was associated with reduced lifespan. Our data reveal that diet composition, alone and in combination with overall caloric intake, modulates lifespan, consumption, and fat deposition in flies, and they provide a useful foundation for dissecting the underlying genetic mechanisms that link specific nutrients with important aspects of general health and longevity.