Project description:The daily intake of dietary fiber is well below the recommended levels in the US. The effect of adopting a low-fat vs. a low-carbohydrate weight loss diet on fiber intake is of interest but not well-documented, especially when both approaches promote high-quality food choices. The objective of this paper is to compare the quantity and sources of dietary fiber between a healthy low-fat (HLF) vs. healthy low-carbohydrate (HLC) diet group when consumed over 12 months in a weight loss diet study. In this secondary analysis of the Diet Intervention Examining The Factors Interacting with Treatment Success (DIETFITS) study, the amount and sources of dietary fiber were examined in generally healthy adults, 18-50 years of age, Body Mass Index (BMI) 28-40 kg/m2, randomized to HLF or HLC for 12 months, who had available 24-h recalls at 0 (n = 609), 3 (n = 549), 6 (n = 491), and 12 (n = 449) months. The dietary intake was estimated by the Nutrition Data System for Research (NDS-R). The sources of fiber were determined for the major food groups. Significantly more total dietary fiber was consumed by HLF at every post-randomization time point, and, at 12 m, was 23.04 ± 9.43 g vs. 18.61 ± 8.12 g for HLF vs. HLC, respectively, p < 0.0001. In both diet groups at 12 months, the highest amount of dietary fiber came from non-starchy vegetables (4.13 ± 3.05 g and 5.13 ± 3.59 g). The other primary sources of fiber at 12 months for the HLF group were from whole grains (3.90 ± 3.13 g) and fruits (3.40 ± 2.87 g), and, for the HLC group, were from plant protein and fat sources, such as nuts and seeds, their butters, and avocados (2.64 ± 2.64 g). In the DIETFITS study, the difference in the total fiber intake for the HLF vs. HLC groups was more modest than expected. The HLC group consumed reasonably high amounts of fiber from high-protein and high fat plant-based sources.
Project description:Diet-induced weight loss in women may be associated with decreases not only in plasma levels of low-density lipoprotein cholesterol (LDL-C), but also in high-density lipoprotein cholesterol (HDL-C). Whether a decrease in HDL-C is associated with altered HDL function is unknown. One hundred overweight or obese women (age 46 ± 11 years, 60 black; 12 diabetic) were enrolled in the 6-month program of reduced fat and total energy diet and low-intensity exercise. Serum cholesterol efflux capacity was measured in (3)H-cholesterol-labeled BHK cells expressing ABCA1, ABCG1, or SR-B1 transporters and incubated with 1% apolipoprotein B (apoB)-depleted serum. Antioxidant properties of HDL were estimated by paraoxonase-1 (PON1) activity and oxygen radical absorbance capacity (ORAC). Endothelial nitric oxide synthase (eNOS) activation was measured by conversion of L-arginine to L-citrulline in endothelial cells incubated with HDL from 49 subjects. Participants achieved an average weight loss of 2.2 ± 3.9 kg (P < 0.001), associated with reductions in both LDL-C (-6 ± 21 mg/dl, P = 0.004) and HDL-C (-3 ± 9 mg/dl, P = 0.016). Cholesterol efflux capacity by the ABCA1 transporter decreased by 10% (P = 0.006); efflux capacities by the ABCG1 and SR-B1 transporters were not significantly altered. ORAC decreased by 15% (P = 0.018); neither PON1 activity nor eNOS activation was significantly altered by reduction in HDL-C. Findings were similar for diabetic and nondiabetic subjects. Diet-induced weight loss in overweight or obese women is associated with a decrease in HDL-C levels, but overall HDL function is relatively spared, suggesting that decrease in HDL-C in this setting is not deleterious to cardiovascular risk.
Project description:Low-fat diets have been shown to increase plasma concentrations of lipoprotein(a) [Lp(a)], a preferential lipoprotein carrier of oxidized phospholipids (OxPLs) in plasma, as well as small dense LDL particles. We sought to determine whether increases in plasma Lp(a) induced by a low-fat high-carbohydrate (LFHC) diet are related to changes in OxPL and LDL subclasses. We studied 63 healthy subjects after 4 weeks of consuming, in random order, a high-fat low-carbohydrate (HFLC) diet and a LFHC diet. Plasma concentrations of Lp(a) (P < 0.01), OxPL/apolipoprotein (apo)B (P < 0.005), and OxPL-apo(a) (P < 0.05) were significantly higher on the LFHC diet compared with the HFLC diet whereas LDL peak particle size was significantly smaller (P < 0.0001). Diet-induced changes in Lp(a) were strongly correlated with changes in OxPL/apoB (P < 0.0001). The increases in plasma Lp(a) levels after the LFHC diet were also correlated with decreases in medium LDL particles (P < 0.01) and increases in very small LDL particles (P < 0.05). These results demonstrate that induction of increased levels of Lp(a) by an LFHC diet is associated with increases in OxPLs and with changes in LDL subclass distribution that may reflect altered metabolism of Lp(a) particles.
Project description:Obesity can lead to ectopic pancreatic fat accumulation and increase the risk for type 2 diabetes. Smaller intervention trials have shown a decrease in pancreatic fat content (PFC) with weight loss, and we intended to investigate the effects of weight loss on PFC in a larger trial. Data from the HELENA-Trial, a randomized controlled trial (RCT) among 137 non-diabetic obese adults were used. The study cohort was classified into 4 quartiles based on weight change between baseline and 12 weeks post-intervention. Changes in PFC (baseline, 12 weeks and 50 weeks post-intervention) upon weight loss were analyzed by linear mixed models. Spearman's coefficients were used to obtain correlations between anthropometric parameters, blood biochemical markers, and PFC. At baseline, PFC only showed a significant correlation with visceral adipose tissue (VAT) (r = 0.41). Relative changes in PFC were significantly (p = 0.01) greater in Q4 (-30.8 ± 5.7%) than in Q1 (1.3 ± 6.7%). These differences remained similar after one year. However, when adjusting the statistical analyses for changes in VAT, the differences in PFC between Q1 and Q4 were no longer statistically significant. Weight loss is associated with a decrease in PFC. However, the reduction of PFC is not independent from reductions in VAT. Unlike VAT, PFC was not associated with metabolic biomarkers.
Project description:BackgroundFor low-carbohydrate diets, a public health approach has focused on the replacement of carbohydrates with unsaturated fats. However, little research exists on the impacts of saturated fat intake on the lipid profile in the context of whole-food-based low-carbohydrate weight-loss diets.ObjectivesThe primary aim of this secondary analysis of the DIETFITS weight loss trial was to evaluate the associations between changes in percentage of dietary saturated fatty acid intake (%SFA) and changes in low-density lipoproteins, high-density lipoproteins, and triglyceride concentrations for those following a healthy low-carbohydrate (HLC) diet. The secondary aim was to examine these associations specifically for HLC dieters who had the highest 12-month increases in %SFA.MethodsIn the DIETFITS trial, 609 generally healthy adults, aged 18-50 years, with body mass indices of 28-40 kg/m2 were randomly assigned to a healthy low-fat (HLF) or HLC diet for 12 months. In this analysis, linear regression, both without and with adjustment for potential confounders, was used to measure the association between 12-month change in %SFA and blood lipids in 208 HLC participants with complete diet and blood lipid data.ResultsParticipants consumed an average of 12-18% of calories from SFA. An increase of %SFA, without significant changes in absolute saturated fat intake, over 12 months was associated with a statistically significant decrease in triglycerides in the context of a weight-loss study in which participants simultaneously decreased carbohydrate intake. The association between increase in %SFA and decrease in triglycerides was no longer significant when adjusting for 12-month change in carbohydrate intake, suggesting carbohydrate intake may be a mediator of this relationship.ConclusionsThose on a low-carbohydrate weight-loss diet who increase their percentage intake of dietary saturated fat may improve their overall lipid profile provided they focus on a high-quality diet and lower their intakes of both calories and refined carbohydrates. This trial was registered at clinicaltrials.gov as NCT01826591.
Project description:Background/objectiveDiet-induced weight loss (WL) leads to increased hunger and reduced fullness feelings, increased ghrelin and reduced satiety peptides concentration (glucagon-like peptide-1 (GLP-1), cholecystokinin (CCK) and peptide YY (PYY)). Ketogenic diets seem to minimise or supress some of these responses. The aim of this study was to determine the timeline over which changes in appetite occur during progressive WL with a ketogenic very-low-energy diet (VLED).Subjects/methodsThirty-one sedentary adults (18 men), with obesity (body mass index: 37±4.5 kg m-2) underwent 8 weeks (wks) of a VLED followed by 4 wks of weight maintenance. Body weight and composition, subjective feelings of appetite and appetite-related hormones (insulin, active ghrelin (AG), active GLP-1, total PYY and CCK) were measured in fasting and postprandially, at baseline, on day 3 of the diet, 5 and 10% WL, and at wks 9 and 13. Data are shown as mean±s.d.ResultsA significant increase in fasting hunger was observed by day 3 (2±1% WL), (P<0.01), 5% WL (12±8 days) (P<0.05) and wk 13 (17±2% WL) (P<0.05). Increased desire to eat was observed by day 3 (P<0.01) and 5% WL (P<0.05). Postprandial prospective food consumption was significantly reduced at wk 9 (16±2% WL) (P<0.01). Basal total PYY was significantly reduced at 10% WL (32±8 days) (P<0.05). Postprandial active GLP-1 was increased at 5% WL (P<0.01) and CCK reduced at 5 and 10% WL (P<0.01, for both) and wk 9 (P<0.001). Basal and postprandial AG were significantly increased at wk 13 (P<0.001, both).ConclusionsWL with a ketogenic VLED transiently increases the drive to eat up to 3 weeks (5% WL). After that, and while participants are ketotic, a 10-17% WL is not associated with increased appetite. However, hunger feelings and AG concentrations increase significantly from baseline, once refeeding occurs.
Project description:ObjectiveThe aim of this study was to determine whether the hormone changes following weight loss are proportional to the degree of weight loss and to starting BMI.MethodsA very low-energy diet was used to achieve 15% weight loss. Fasting and postprandial gut hormones and leptin were measured during a meal test at baseline and at 5% (1%), 10% (2%), and 15% (2.5%) weight loss. Linear mixed-effects models were used to analyze hormone changes.ResultsFrom baseline to 5% weight loss, decreases were seen in fasting concentrations of leptin (-8.25 ng/mL; p < 0.001), amylin (-21.3 pg/mL; p < 0.001), and glucagon-like peptide 1 (-59.55 pg/mL; p < 0.001). There was a small further reduction in leptin between 5% and 15% weight loss (-1.88 ng/mL; p = 0.019) but not in glucagon-like peptide 1 and amylin. Fasting ghrelin showed a significant increase at 10% weight loss (41.64 pg/mL; p = 0.002), with a nonsignificant increase from 10% to 15% loss (26.03 pg/mL; p = 0.065). Postprandial changes in hormone levels were variable. There was no correlation between baseline weight and the degree of hormone changes.ConclusionsThe majority of changes in fasting gut hormones and leptin occurred in early weight loss, with minor further changes up to 15% weight loss. Starting weight did not affect the degree of hormone change.
Project description:ObjectiveAtherosclerosis, a chronic inflammatory disease, arises from metabolic disorders and is driven by inappropriate recruitment and proliferation of monocytes / macrophages and vascular smooth-muscle-cells. The receptor for the urokinase-type plasminogen activator (uPAR, Plaur) regulates the proteolytic activation of plasminogen. It is also a coactivator of integrins and facilitates leukocyte-endothelial interactions and vascular smooth-muscle-cell migration. The role of uPAR in atherogenesis remains elusive.Methods and resultsWe generated C57Bl6/J low-density lipoprotein receptor (LDL) and uPAR double knockout (uPAR-/-/LDLR-/-) mice to test the role of uPAR in two distinct atherosclerosis models. In LDLR-/- mice, hepatic overexpression following hydrodynamic transfection of soluble uPAR that competes with endogenous membrane-bound uPAR was performed as an interventional strategy. Aortic root atherosclerotic lesions induced by feeding a high-fat diet were smaller and comprised less macrophages and vascular smooth-muscle-cells in double knockout mice and animals overexpressing soluble uPAR when compared to controls. In contrast, lesion size, lipid-, macrophage-, and vascular smooth muscle cell content of guide-wire-induced intima lesions in the carotid artery were not affected by uPAR deficiency. Adhesion of uPAR-/--macrophages to TNFα-stimulated endothelial cells was decreased in vitro accompanied by reduced VCAM-1 expression on primary endothelial cells. Hepatic overexpression of soluble full-length murine uPAR in LDLR-/- mice led to a reduction of diet-induced atherosclerotic lesion formation and monocyte recruitment into plaques. Ex vivo incubation with soluble uPAR protein also inhibited adhesion of macrophages to TNFα-stimulated endothelial cells in vitro.ConclusionuPAR-deficiency as well as competitive soluble uPAR reduced diet-promoted but not guide-wire induced atherosclerotic lesions in mice by preventing monocyte recruitment and vascular smooth-muscle-cell infiltration. Soluble uPAR may represent a therapeutic tool for the modulation of hyperlipidemia-associated atherosclerotic lesion formation.
Project description:BackgroundReductions in energy intake are seen in weight loss trials, but whether this occurs with improvements to diet quality (DQ) is less established. The aim of this study was to evaluate changes in diet quality in a sample of volunteers in a weight loss trial.MethodsThis was a secondary analysis of dietary data from a lifestyle intervention trial (the HealthTrack study) which advised on dietary guidelines. The trial ran for 12 months with three treatment groups: control (general advice C), intervention (individualised advice, I), and intervention plus a supplement of walnuts (IW). Both the published a priori diet quality score (APDQS, maximum score 164) and a study specific Diet Quality Tracker (DQT, maximum score 44) indicated compliance to dietary advice. DQ scores calculated at 0, 3months and 12months were evaluated using two-way RMANOVA, one-way ANOVA and one-way RMANOVA. Changes in intakes of food groups and nutrients were analysed using Kruskal-Wallis and Friedman's tests.ResultsThere were no differences between groups at baseline, but at 3months IW recorded higher DQ scores (APDQS:96 ± 10; DQT:22 ± 5, P < 1 × 10-3 for both) compared to I (APDQS:91 ± 13, P < 1 × 10-3; DQT:21 ± 4, P < 1 × 10-2) and C (APDQS:87 ± 12, P < 5 × 10-2; DQT:19 ± 4, P > 5 × 10-2), and a higher consumption of nuts at 3 months (P < 1 × 10-3), and 12months (P < 1 × 10-2). All groups reported decreased intakes of discretionary foods/beverages assessed by the DQT (P < 1 × 10-3 for IW and I; P < 1 × 10-2 for C). The APDQS showed this as reduced intakes of grain based desserts (P < 1 × 10-3 at 3 and 12months), and salty snacks at 12months (P < 1 × 10-3 for IW and I; P < 5 × 10-2 for C). Intakes of monounsaturated and saturated fatty acids were lowest, and polyunsaturated fatty acids highest for IW (P < 1 × 10-3), resulting in a higher dietary polyunsaturated:saturated fat ratio (P < 1 × 10-3).ConclusionsLifestyle intervention addressing dietary guidelines can lead to significant reductions in consumption of discretionary foods and saturated fat, but individualised advice may have a greater impact on improving overall DQ regardless of DQI used. Providing a healthy food supplement may help assure higher DQ and where the food is walnuts, produce commensurate differences in dietary fatty acid profiles.Trial registrationANZCTRN 12614000581662. Date of registration: 30th May 2014.
Project description:BackgroundAccruing evidence indicates that accumulation of advanced glycation end products (AGEs) and activation of the receptor for AGEs (RAGE) play a significant role in obesity and type 2 diabetes. The concentrations of circulating RAGE isoforms, such as soluble RAGE (sRAGE), cleaved RAGE (cRAGE), and endogenous secretory RAGE (esRAGE), collectively sRAGE isoforms, may be implicit in weight loss and energy compensation resulting from caloric restriction.ObjectivesWe aimed to evaluate whether baseline concentrations of sRAGE isoforms predicted changes (∆) in body composition [fat mass (FM), fat-free mass (FFM)], resting energy expenditure (REE), and adaptive thermogenesis (AT) during weight loss.MethodsData were collected during a behavioral weight loss intervention in adults with obesity. At baseline and 3 mo, participants were assessed for body composition (bioelectrical impedance analysis) and REE (indirect calorimetry), and plasma was assayed for concentrations of sRAGE isoforms (sRAGE, esRAGE, cRAGE). AT was calculated using various mathematical models that included measured and predicted REE. A linear regression model that adjusted for age, sex, glycated hemoglobin (HbA1c), and randomization arm was used to test the associations between sRAGE isoforms and metabolic outcomes.ResultsParticipants (n = 41; 70% female; mean ± SD age: 57 ± 11 y; BMI: 38.7 ± 3.4 kg/m2) experienced modest and variable weight loss over 3 mo. Although baseline sRAGE isoforms did not predict changes in ∆FM or ∆FFM, all baseline sRAGE isoforms were positively associated with ∆REE at 3 mo. Baseline esRAGE was positively associated with AT in some, but not all, AT models. The association between sRAGE isoforms and energy expenditure was independent of HbA1c, suggesting that the relation was unrelated to glycemia.ConclusionsThis study demonstrates a novel link between RAGE and energy expenditure in human participants undergoing weight loss.This trial was registered at clinicaltrials.gov as NCT03336411.