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Abstract Background Very little is known about the longitudinal changes in energy requirements in late life. The purposes of this study were to: (1) determine the energy requirements in late life and how they changed during a 7 year time-span, (2) determine whether changes in fat free mass (FFM) were related to changes in resting metabolic rate (RMR), and (3) determine the accuracy of predicted total energy expenditure (TEE) to measured TEE. Methods TEE was assessed via doubly labeled water (DLW) technique in older adults in both 1999 (n = 302; age: 74 ± 2.9 yrs) and again in 2006 (n = 87 age: 82 ± 3.1 yrs). RMR was measured with indirect calorimetry, and body composition was assessed with dual-energy x-ray absorptiometry. Results The energy requirements in the 9th decade of life were 2208 ± 376 kcal/d for men and 1814 ± 337 kcal/d for women. This was a significant decrease from the energy requirements in the 8th decade of life in men (2482 ± 476 kcal/d vs. 2208 ± 376 kcal/d) but not in women (1892 ± 271 kcal/d vs. 1814 ± 337 kcal/d). In addition to TEE, RMR, and activity EE (AEE) also decreased in men, but not women, while FFM decreased in both men and women. The changes in FFM were correlated with changes in RMR for men (r = 0.49, p

Background: Differences in metabolic responses between diets rich in monounsaturated fatty acid (MUFA) and polyunsaturated fatty acid (PUFA) could affect energy balance and weight maintenance. The present study was a secondary analysis to investigate 8‐week diet interventions rich in either PUFA (cottonseed oil [CSO]) or MUFA (olive oil [OO]) on metabolic responses in adults with dyslipidaemia. Methods: Forty‐one adults with dyslipidaemia completed this randomised trial consisting of an 8‐week partial‐outpatient feeding trial. Provided foods accounted for about 60% of their daily energy needs, with about 30% of energy needs provided by CSO (n = 20) or OO (n = 21). At pre‐ and postdiet intervention visits, participants consumed a high saturated fatty acid (SFA) meal (35% daily energy needs, 47.9% from SFA), and fasting and 3.5‐h postprandial indirect calorimetry were used to measure energy expenditure (EE) and substrate oxidation. Results: No changes were observed in fasting measures. The OO group had greater increases in postprandial EE (p = 0.002); however, there were no differences in substrate oxidation between groups. A lack of metabolic flexibility was found in both groups, which was partially explained by changes in insulin sensitivity (homeostasis model assessment of insulin resistance). Conclusions: The results of the present study show that OO, but not CSO, diet enrichment improves EE after an occasional high SFA meal, which may improve weight maintenance over time. This study is registered at clinicaltrials.gov (NCT04397055). Key points: An olive‐oil‐enriched diet may improve postmeal energy expenditure more than a cottonseed‐oil‐enriched diet.Exploratory analysis suggests that changes in insulin resistance (homeostasis model assessment of insulin resistance) may contribute to one's ability to adapt to a high‐fat diet. [ABSTRACT FROM AUTHOR]

Background: Research indicates that diets enriched with unsaturated fatty acids improve energy metabolism, although studies on tree nuts, which are a rich source of those fats, are limited. The present study aimed to examine the impact of daily pecan consumption for 8 weeks on energy metabolism in adults with hypercholesterolaemia or at higher risk for cardiovascular disease (CVD) (body mass index ≥ 28 kg m–2). Methods: For this randomised, controlled trial, 56 sedentary adults were randomised into one of three treatments for an 8‐week intervention: two pecan groups and a nut‐free control group (n = 18). The ADD group (n = 16) consumed pecans as part of a free‐living diet, whereas the SUB group (n = 18) substituted the pecans for isocaloric foods from their habitual diet. At baseline and 8 weeks, a high saturated fat meal was consumed along with indirect calorimetry measurements at fasting and for 4 h postprandially to determine changes in resting metabolic rate (RMR), diet induced thermogenesis (DIT) and substrate utilisation (primary outcomes). Forty‐seven participants completed the trial and were included in analyses. Results: In the SUB group, there was an increase in fasting RMR (1607 ± 117 to 1701 ± 114 kcal day–1; p = 0.01) and fasting fat oxidation (0.83 ± 0.08 to 0.99 ± 0.08 g/15 min; p = 0.009) and a decrease in fasting respiratory exchange ratio (0.85 ± 0.01 to 0.83 ± 0.01; p = 0.05) from pre‐ to post‐intervention. In the ADD group, there was an increase in postprandial DIT (p < 0.001). There were no changes within the control group or between groups for any outcome measure. Conclusions: Daily consumption of pecans may increase select measures of energy expenditure and fat oxidation in adults at‐risk for CVD. Key points: Daily consumption of pecans may improve select measures of energy expenditure or fat metabolism.When consuming pecans daily, the presence or absence of dietary substitution instructions may be an important determinant of energy metabolism outcomes. [ABSTRACT FROM AUTHOR]

Stearoyl-CoA desaturase-1 (SCD-1) is the rate-limiting enzyme in the biosynthesis of monounsaturated fatty acids (MUFA), which are required for efficient neutral lipid esterification. In the present investigation, we demonstrate that loss of SCD-1 activity increases free cholesterol (FC) content and induces Xbp-1 splicing. We assessed the small molecule SCD-1 inhibitor A939572 on [[sup.14]C]stearate incorporation into neutral lipids and found its incorporation into triglyceride was unaffected, whereas labeled cholesteryl ester (CE) content was notably diminished. Using either A939572 or liver knockout mice (LKO), we show that loss of SCD-1 activity increases FC levels and activates the liver X receptor (LXR) pathway. Using adenoviral delivery of an active form of X-box binding protein-1 (Xbp-1; Xbp-1s), we show increased sterol synthesis only when cells lack the ability to generate MUFA. The results of the cell-based model were confirmed in LKO mice where fasting-refeeding decreased CE, increased FC, and increased Xbp-1s. On the basis of the present data, we conclude that SCD-1 activity is required for efficient cholesterol esterification to MUFA and that loss of its activity increases Xbp-1s-mediated FC synthesis. It is likely that the accumulation of FC enhances Xbp-1 splicing, induces LXR transcriptional activity, and increases ABCA1 (ATP-binding cassette transporter A1) expression to maintain cholesterol homeostasis. cell stress; fasting-refeeding; cholesterol metabolism; acyl-coenzyme A:cholesterol acyltransferase-1; X-box binding protein-1; caveolin-1 doi: 10.1152/ajpendo.00388.2010.

A key and highly regulated enzyme that is required for the biosynthesis of monounsaturated fatty acids is stearoyl-CoA desaturase (SCD), which catalyzes the [D.sup.9]-cis desaturation of a range of fatty acyl-CoA substrates. The preferred substrates are palmitoyl- and stearoyl-CoA, which are converted into palmitoleoyl- and oleoyl-CoA respectively. Oleate is the most abundant monounsaturated fatty acid in dietary fat and is therefore readily available. Studies of mice that have a naturally occurring mutation in the SCD-1 gene isoform as well as a mouse model with a targeted disruption of the SCD gene (SCD-[1.sup.-/-]) have revealed the role of de novo synthesized oleate and thus the physiological importance of SCD-1 expression. SCD-1 deficiency results in reduced body adiposity, increased insulin sensitivity, and resistance to diet-induced obesity. The expression of several genes of lipid oxidation are upregulated, whereas lipid synthesis genes are downregulated. SCD-1 was also found to be a component of the novel metabolic response to the hormone leptin. Therefore, SCD-1 appears to be an important metabolic control point, and inhibition of its expression could be of benefit for the treatment of obesity, diabetes, and other metabolic diseases. In this article, we summarize the recent and timely advances concerning the important role of SCD in the biochemistry and physiology of lipid metabolism.

In its role as an endothelial cell proliferation and migration factor, vascular endothelial growth factor (VEGF) can affect peripheral circulation and therefore impact maximal oxygen consumption (V[O.sub.2 max]). Because of the role of VEGF, and because variation in the VEGF gene has the ability to alter VEGF gene expression and VEGF protein level, we hypothesized that VEGF gene polylnorphisms are related to VEGF gene expression in human myoblasts and V[O.sub.2 max] before and after aerobic exercise training. We analyzed the effects of the VEGF -2578/ -1154/-634 protnoter region haplotype on VEGF gene expression by using a luciferase reporter assay in cultured human myoblasts and found that the AAG and CGC haplotypes resulted m significantly higher hypoxia-stimulated VEGF gene expression than the AGG and CGG haplotypes. Consistent with these results, we found that individuals with at least one copy of the AAG or CGC haplotype had higher V[O.sub.2 max] before and after aerobic exercise training than did subjects with only the AGG and/or CGG haplotype. In conclusion, we found that VEGF-2578/-1154/-634 haplotype impacts VEGF gene expression in human myoblasts and is associated with V[O.sub.2 max]. These results have potential implications for aerobic exercise training and may prove relevant in the study of pathological conditions that can be affected by angiogenesis, such as coronary artery disease and peripheral artery disease. angiogenesis; exercise; genetics; polymorphism