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Longitudinal association of dietary carbohydrate quality with visceral fat deposition and other adiposity indicators.
Zamanillo-Campos, R, Chaplin, A, Romaguera, D, Abete, I, Salas-Salvadó, J, Martín, V, Estruch, R, Vidal, J, Ruiz-Canela, M, Babio, N, et al
Clinical nutrition (Edinburgh, Scotland). 2022;41(10):2264-2274
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Abdominal obesity, measured by waist circumference, a proxy of visceral fat, is increasing at an even greater rate than overall obesity alone. Diet plays a key role in body fat accumulation; however, recent evidence also indicates that, beyond quantity, the quality of certain nutrients may have an independent effect. The aim of this study was to determine the dynamic association between changes in overall dietary carbohydrate quality and changes in objectively measured visceral and overall adiposity distribution This study is a prospective cohort study based on data collected during the first year of the PREDIMED-Plus (PREvencion con DIeta MEDiterranea Plus) randomised controlled trial. In the PREDIMED-Plus trial, a total of 6874 people were randomly allocated in a 1:1 ratio to either the intervention or control group. Results show that a carbohydrate quality index increase was associated with a decrease in regional and overall adiposity. The observed associations were mostly driven by fibre and the wholegrains/total grains ratio. Authors conclude that the promotion of fibre-rich foods, including fruits, vegetables, legumes and nuts, and the substitution of refined grains by wholegrains, may be important dietary recommendations to adopt in clinical practice to promote a healthier body composition.
Expert Review
Conflicts of interest:
None
Take Home Message:
This prospective cohort of older adults with overweight/obesity and MetS, found that improvements in dietary carbohydrate quality over one year was associated with positive changes in visceral and overall fat deposition, largely due to dietary fibre and the wholegrain/total grain ratio.
Evidence Category:
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A: Meta-analyses, position-stands, randomized-controlled trials (RCTs)
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B: Systematic reviews including RCTs of limited number
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C: Non-randomized trials, observational studies, narrative reviews
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D: Case-reports, evidence-based clinical findings
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E: Opinion piece, other
Summary Review:
Background
Obesity prevalence is increasing worldwide and is associated with a range of metabolic and cardiovascular diseases. Excess visceral fat appears with increasing age but also with unhealthy dietary patterns and lifestyle behaviours, and it contributes to chronic diseases, particularly type 2 diabetes (T2D), insulin resistance, metabolic syndrome (MetS), and cardiovascular diseases (CVD).
Aim
This study determined the association between changes in overall dietary carbohydrate quality and changes in objectively-measured visceral and overall adiposity distribution. Three repeated measurements of diet and adiposity were conducted throughout a 1-year follow-up, using a dual-energy X-ray absorptiometry (DXA) scans for body composition assessment.
The study compared an intensive weight-loss (intervention group) using an energy-reduced Mediterranean Diet (MedDiet), with physical activity (PA), and behavioural support on the prevention of CVD events, compared to usual care and dietary counselling only.
This prospective cohort study analysed a subgroup of 1476 participants (men aged 55-75 years and women aged 60-75 years) enrolled in the PREDIMED-Plus randomized controlled trial. Participants were overweight or obese (BMI>27 kg/m2 and <40 kg/m2) with no previous cardiovascular events and at least three characteristics of metabolic syndrome (MetS): hypertension, hyper-triglyceridemia, lower high-density lipoprotein (HDL) cholesterol, hyperglycemia, or central obesity.
Dietary intake was measured at baseline, 6- and 12-months using a Spanish version of the validated 143-item semi-quantitative food-frequency questionnaire, via face-to-face interviews by trained dietitian-nutritionists. Carbohydrate quality index (CQI) was calculated using four criteria: total dietary fibre, glycemic index, wholegrain/total grain carbohydrate ratio, and solid/total carbohydrate ratio.
Results
Improvements in body composition and lifestyle factors were observed compared to baseline data (both study arms combined) (p < 0.05 for all). A higher Carbohydrate Quality Index CQI (p = 0.024) was observed at both the 6 and 12 month follow-up.
A 3-point increment in CQI over 12-month follow-up was associated with a decrease in visceral fat (β 0.067 z-score, 95% CI -0.088 to -0.046, p<0.001), android-to-gynoid fat ratio* (β -0.038, 95% CI -0.059 to -0.017, p<0.001) (*calculated by dividing the fat mass (g) from the specific regions), and total fat (β -0.064, 95% CI -0.080 to -0.047, p<0.001).
Fibre intake and the ratio of whole grain/total grain showed the strongest inverse associations with all adiposity indicators. Statistically significant differences were observed over time in all CQI components. The most relevant changes were the increase in consumption of carbohydrates from whole-grains and a decrease in refined grains, and an increase in dietary fibre intake. After evaluating each CQI component separately, the study found that fibre intake and the ratio of whole grain/total grain presented the strongest and statistically significant negative associations with all adiposity indicators (all p-values <0.01).
Limitations
Due to the observational nature of the study, causality cannot be inferred. The study population is based on older people with overweight/obesity and MetS from a Mediterranean area, which can limit the generalisability of findings to the general population.
The use of self-reported dietary data is subject to measurement error, where self-reports may be affected by a tendency to respond in a manner to avoid criticism or judgement and to seek social approval.
Clinical practice applications:
Evidence has shown that the quality of dietary carbohydrates, rather than the quantity, may have a greater impact on health and overall mortality.
While visceral fat constitutes only a small proportion of total fat, the available evidence indicates that it plays an important role in certain chronic diseases, such as T2D, MetS, CVD and cancer.
Findings from this study suggest a better CQI via the manipulation of carbohydrate quality may be associated with a decrease in visceral fat, which are independent of changes in total body fat.
Considerations for future research:
Future strategies to decrease visceral fat are warranted.
Robust reference ranges are needed for the interpretation of visceral fat in clinical practice and research settings.
Abstract
BACKGROUND & AIMS The quality of dietary carbohydrates rather than total carbohydrate intake may determine the accumulation of visceral fat; however, to date, few studies have examined the impact of diet on adiposity using specific imaging techniques. Thus, the aim of this prospective study was to investigate the association between concurrent changes in carbohydrate quality index (CQI) and objectively-quantified adiposity distribution over a year. METHODS We analyzed a cohort of 1476 participants aged 55-75 years with overweight/obesity and metabolic syndrome (MetS) from the PREDIMED-Plus randomized controlled trial. Dietary intake information was obtained at baseline, 6- and 12-months from a validated 143-item semi-quantitative food-frequency questionnaire, and CQI (range: 4 to 20) was calculated based on four dietary criteria: total dietary fibre, glycemic index, wholegrain/total grain carbohydrate ratio, and solid/total carbohydrate ratio. Overall and regional adiposity (total body fat, visceral fat and android-to-gynoid fat ratio) was quantified using dual-energy X-ray absorptiometry at all three time points. Multiple adjusted linear mixed-effects models were used to assess associations between concurrent changes in repeatedly measured CQI and adiposity over time. RESULTS After controlling for potential confounding factors, a 3-point increment in CQI over 12-month follow-up was associated with a decrease in visceral fat (β -0.067 z-score, 95% CI -0.088; -0.046, p < 0.001), android-to-gynoid fat ratio (-0.038, -0.059; -0.017, p < 0.001), and total fat (-0.064, -0.080; -0.047, p < 0.001). Fibre intake and the ratio of wholegrain/total grain showed the strongest inverse associations with all adiposity indicators. CONCLUSIONS In this prospective cohort of older adults with overweight/obesity and MetS, we found that improvements in dietary carbohydrate quality over a year were associated with concurrent favorable changes in visceral and overall fat deposition. These associations were mostly driven by dietary fibre and the wholegrain/total grain ratio. TRIAL REGISTRATION The trial was registered at the International Standard Randomized. CONTROLLED TRIAL (ISRCTN http://www.isrctn.com/ISRCTN89898870) with number 89898870 and registration date of 24 July 2014, retrospectively registered.
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Weight Loss and Exercise Differentially Affect Insulin Sensitivity, Body Composition, Cardiorespiratory Fitness, and Muscle Strength in Older Adults With Obesity: A Randomized Controlled Trial.
Brennan, AM, Standley, RA, Anthony, SJ, Grench, KE, Helbling, NL, DeLany, JP, Cornnell, HH, Yi, F, Stefanovic-Racic, M, Toledo, FGS, et al
The journals of gerontology. Series A, Biological sciences and medical sciences. 2022;77(5):1088-1097
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Aging is marked by increased risk for type 2 diabetes, reduced muscle mass and strength (ie, sarcopenia), decreased physical function and cardiorespiratory fitness, ectopic fat deposition, and insulin resistance all of which increase the risk for physical disability, morbidity, and mortality. These adverse health consequences associated with advanced age are exacerbated with obesity and physical inactivity. The aim of this study was to investigate the effects of weight loss with or without exercise on skeletal muscle insulin sensitivity, exclusively in obese older adults. This study is a 2-site, 6-month randomized controlled trial with a parallel group design. Eighty-six older (60–80 years of age), physically inactive men and women with obesity were randomised into one of the 3 treatments (1:1:1 allocation ratio): control (health education), calorie restriction-induced weight loss, and weight loss with exercise. Results suggest that weight loss via calorie restriction alone is insufficient to significantly improve skeletal muscle insulin sensitivity and requires the addition of exercise to incur benefit, which was also true for clinical measures of insulin resistance including haemoglobin A1C [a blood test that measures the average blood sugar levels over a period of 3 months] and fasting insulin. Authors conclude that regular exercise should be considered as a useful and manageable adjunct to traditional weight loss therapies for older adults with obesity to mitigate risk for chronic disease and maintain functional independence and quality of life.
Abstract
BACKGROUND Aging-related disease risk is exacerbated by obesity and physical inactivity. It is unclear how weight loss and increased activity improve risk in older adults. We aimed to determine the effects of diet-induced weight loss with and without exercise on insulin sensitivity, VO2peak, body composition, and physical function in older obese adults. METHODS Physically inactive older (68.6 ± 4.5 years) obese (body mass index 37.4 ± 4.9 kg/m2) adults were randomized to health education control (HEC; n = 25); diet-induced weight loss (WL; n = 31); or weight loss and exercise (WLEX; n = 28) for 6 months. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp, body composition by dual-energy X-ray absorptiometry and MRI, strength by isokinetic dynamometry, and VO2peak by graded exercise test. RESULTS WLEX improved (p < .05) peripheral insulin sensitivity (+75 ± 103%) versus HEC (+12 ± 67%); WL (+36 ± 47%) versus HEC did not reach statistical significance. WLEX increased VO2peak (+7 ± 12%) versus WL (-2 ± 24%) and prevented reductions in strength and lean mass induced by WL (p < .05). WLEX decreased abdominal adipose tissue (-16 ± 9%) versus HEC (-3 ± 8%) and intermuscular adipose tissue (-15 ± 13%) versus both HEC (+9 ± 15%) and WL (+2 ± 11%; p < .01). CONCLUSIONS Exercise with weight loss improved insulin sensitivity and VO2peak, decreased ectopic fat, and preserved lean mass and strength. Weight loss alone decreased lean mass and strength. Older adults intending to lose weight should perform regular exercise to promote cardiometabolic and functional benefits, which may not occur with calorie restriction-induced weight loss alone.
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A high-carbohydrate diet lowers the rate of adipose tissue mitochondrial respiration.
Bikman, BT, Shimy, KJ, Apovian, CM, Yu, S, Saito, ER, Walton, CM, Ebbeling, CB, Ludwig, DS
European journal of clinical nutrition. 2022;76(9):1339-1342
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The hormone insulin plays a fundamental role in cellular nutrient signalling, including mitochondrial function. The aim of this study was to test the hypothesis that a high-carbohydrate diet would lower measures of mitochondrial respiration in adipose tissue, consistent with the carbohydrate-insulin model of obesity. This study is an ancillary study of the Framingham State Food Study, in which the primary outcome was total energy expenditure. Data of twenty-seven participants were included in this report. Results show that a high-carbohydrate diet lowers mitochondrial respiratory function. Authors conclude the study’s sample may not reflect mitochondrial activity in all body fat depots. Thus, further research is required in order to replicate the study’s findings, conduct quantitative energetic studies, examine generalizability to other populations and experimental conditions, and explore translation to the prevention and treatment of obesity.
Abstract
Adipocyte mitochondrial respiration may influence metabolic fuel partitioning into oxidation versus storage, with implications for whole-body energy expenditure. Although insulin has been shown to influence mitochondrial respiration, the effects of dietary macronutrient composition have not been well characterized. The aim of this exploratory study was to test the hypothesis that a high-carbohydrate diet lowers the oxygen flux of adipocyte mitochondria ex vivo. Among participants in a randomized-controlled weight-loss maintenance feeding trial, those consuming a high-carbohydrate diet (60% carbohydrate as a proportion of total energy, n = 10) had lower rates of maximal adipose tissue mitochondrial respiration than those consuming a moderate-carbohydrate diet (40%, n = 8, p = 0.039) or a low-carbohydrate diet (20%, n = 9, p = 0.005) after 10 to 15 weeks. This preliminary finding may provide a mechanism for postulated calorie-independent effects of dietary composition on energy expenditure and fat deposition, potentially through the actions of insulin on fuel partitioning.
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Linoleic Acid-Rich Oil Alters Circulating Cardiolipin Species and Fatty Acid Composition in Adults: A Randomized Controlled Trial.
Cole, RM, Angelotti, A, Sparagna, GC, Ni, A, Belury, MA
Molecular nutrition & food research. 2022;66(15):e2101132
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Dietary polyunsaturated fatty acid intake is associated with reduced cardiometabolic disease risk. In addition, higher linoleic acid (LA) biomarkers have been associated with a reduced risk for cardiometabolic diseases and conditions. The main aim of this study was to determine whether a modest addition of an oil rich in LA could change the LA content in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMCs). The secondary aim was to determine if the LA-rich oil could alter cardiolipin species in PBMCs. This study is a randomised double-masked placebo-controlled study of 84 participants who were randomly assigned to one of the two groups: either the high-oleate-cookie (n = 42) or LA-cookie groups (n = 42). Results show that dietary supplementation with less than one serving of LA-rich oil per day increases LA in PBMC cardiolipin as well as LA levels. Authors conclude that patients with obesity, cardiometabolic disease, and other conditions related to mitochondrial dysfunction could be a future cohort that should be studied.
Abstract
SCOPE Higher circulating linoleic acid (LA) and muscle-derived tetralinoleoyl-cardiolipin (LA4 CL) are each associated with decreased cardiometabolic disease risk. Mitochondrial dysfunction occurs with low LA4 CL. Whether LA-rich oil fortification can increase LA4 CL in humans is unknown. The aims of this study are to determine whether dietary fortification with LA-rich oil for 2 weeks increases: 1) LA in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMC); and 2) LA4 CL in PBMC in adults. METHODS AND RESULTS In this randomized controlled trial, adults are instructed to consume one cookie per day delivering 10 g grapeseed (LA-cookie, N = 42) or high oleate (OA) safflower (OA-cookie, N = 42) oil. In the LA-cookie group, LA increases in plasma, erythrocyte, and PBMC by 6%, 7%, and 10% respectively. PBMC and erythrocyte OA increase by 7% and 4% in the OA-cookie group but is unchanged in the plasma. PBMC LA4 CL increases (5%) while LA3 OA1 CL decreases (7%) in the LA-cookie group but are unaltered in the OA-cookie group. CONCLUSIONS LA-rich oil fortification increases while OA-oil has no effect on LA4 CL in adults. Because LA-rich oil fortification reduces cardiometabolic disease risk and increases LA4 CL, determining whether mitochondrial dysfunction is repaired through dietary fortification is warranted.
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Effects of a low-carbohydrate diet on insulin-resistant dyslipoproteinemia-a randomized controlled feeding trial.
Ebbeling, CB, Knapp, A, Johnson, A, Wong, JMW, Greco, KF, Ma, C, Mora, S, Ludwig, DS
The American journal of clinical nutrition. 2022;115(1):154-162
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Diets high in carbohydrates and particularly processed carbohydrates can increase the risk for developing a dysfunction in the body’s ability to take up sugar from the blood, known as insulin resistance. However how this relates to insulin resistance can contribute to the development of many diseases such as type 2 diabetes, heart disease and stroke, which highlights the importance in preventing this dysfunction. This randomised control trial of 148 individuals aimed to determine the role of low, medium, and high carbohydrate diets with varying saturated fat content on measures for insulin resistance. The results showed that regardless of the fat content, it was the level of carbohydrate that determined the effect on measures of insulin resistance. High saturated fat and low-carbohydrate diets improved insulin resistance and low saturated fat high carbohydrate diets worsened insulin resistance. Improvements were also observed in blood lipids with a high fat low carbohydrate diet. It was concluded that a diet low in carbohydrates, but high in saturated fat improved insulin resistance and blood lipid levels. This study could be used by healthcare professionals to understand that a diet, which replaces fat with carbohydrates may be worsening insulin resistance and that low carbohydrate diets may be of benefit.
Abstract
BACKGROUND Carbohydrate restriction shows promise for diabetes, but concerns regarding high saturated fat content of low-carbohydrate diets limit widespread adoption. OBJECTIVES This preplanned ancillary study aimed to determine how diets varying widely in carbohydrate and saturated fat affect cardiovascular disease (CVD) risk factors during weight-loss maintenance. METHODS After 10-14% weight loss on a run-in diet, 164 participants (70% female; BMI = 32.4 ± 4.8 kg/m2) were randomly assigned to 3 weight-loss maintenance diets for 20 wk. The prepared diets contained 20% protein and differed 3-fold in carbohydrate (Carb) and saturated fat as a proportion of energy (Low-Carb: 20% carbohydrate, 21% saturated fat; Moderate-Carb: 40%, 14%; High-Carb: 60%, 7%). Fasting plasma samples were collected prerandomization and at 20 wk. Lipoprotein insulin resistance (LPIR) score was calculated from triglyceride-rich, high-density, and low-density lipoprotein particle (TRL-P, HDL-P, LDL-P) sizes and subfraction concentrations (large/very large TRL-P, large HDL-P, small LDL-P). Other outcomes included lipoprotein(a), triglycerides, HDL cholesterol, LDL cholesterol, adiponectin, and inflammatory markers. Repeated measures ANOVA was used for intention-to-treat analysis. RESULTS Retention was 90%. Mean change in LPIR (scale 0-100) differed by diet in a dose-dependent fashion: Low-Carb (-5.3; 95% CI: -9.2, -1.5), Moderate-Carb (-0.02; 95% CI: -4.1, 4.1), High-Carb (3.6; 95% CI: -0.6, 7.7), P = 0.009. Low-Carb also favorably affected lipoprotein(a) [-14.7% (95% CI: -19.5, -9.5), -2.1 (95% CI: -8.2, 4.3), and 0.2 (95% CI: -6.0, 6.8), respectively; P = 0.0005], triglycerides, HDL cholesterol, large/very large TRL-P, large HDL-P, and adiponectin. LDL cholesterol, LDL-P, and inflammatory markers did not differ by diet. CONCLUSIONS A low-carbohydrate diet, high in saturated fat, improved insulin-resistant dyslipoproteinemia and lipoprotein(a), without adverse effect on LDL cholesterol. Carbohydrate restriction might lower CVD risk independently of body weight, a possibility that warrants study in major multicentered trials powered on hard outcomes. The registry is available through ClinicialTrials.gov: https://clinicaltrials.gov/ct2/show/NCT02068885.
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Lipids activate skeletal muscle mitochondrial fission and quality control networks to induce insulin resistance in humans.
Axelrod, CL, Fealy, CE, Erickson, ML, Davuluri, G, Fujioka, H, Dantas, WS, Huang, E, Pergola, K, Mey, JT, King, WT, et al
Metabolism: clinical and experimental. 2021;121:154803
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Insulin resistance is a key pathophysiological mechanism in the development and progression of type 2 diabetes. Abnormalities in lipid metabolism and ectopic lipid accumulation are known to directly contribute to the onset of insulin resistance. Authors hypothesised that lipid infusion would increase dynamin related protein 1 [a type of protein]-mediated mitochondrial fission in skeletal muscle independent of function and content, consequently reducing peripheral insulin sensitivity. The study included sedentary but otherwise healthy adults who were prospectively randomized to receive either lipid or saline infusion to isolate the direct contribution of fatty acids to skeletal muscle mitochondrial dynamics. Results show that mitochondrial fission and quality control networks are activated in response to lipid infusion which occurs independent of changes in mitochondrial content or capacity and contributes to the onset of insulin resistance in healthy humans. Authors conclude that treatments that limit lipid-induced activation of mitochondrial fission and/or quality control processes may have therapeutic value in the treatment of insulin resistance.
Abstract
BACKGROUND AND AIMS A diminution in skeletal muscle mitochondrial function due to ectopic lipid accumulation and excess nutrient intake is thought to contribute to insulin resistance and the development of type 2 diabetes. However, the functional integrity of mitochondria in insulin-resistant skeletal muscle remains highly controversial. METHODS 19 healthy adults (age:28.4 ± 1.7 years; BMI:22.7 ± 0.3 kg/m2) received an overnight intravenous infusion of lipid (20% Intralipid) or saline followed by a hyperinsulinemic-euglycemic clamp to assess insulin sensitivity using a randomized crossover design. Skeletal muscle biopsies were obtained after the overnight lipid infusion to evaluate activation of mitochondrial dynamics proteins, ex-vivo mitochondrial membrane potential, ex-vivo oxidative phosphorylation and electron transfer capacity, and mitochondrial ultrastructure. RESULTS Overnight lipid infusion increased dynamin related protein 1 (DRP1) phosphorylation at serine 616 and PTEN-induced kinase 1 (PINK1) expression (P = 0.003 and P = 0.008, respectively) in skeletal muscle while reducing mitochondrial membrane potential (P = 0.042). The lipid infusion also increased mitochondrial-associated lipid droplet formation (P = 0.011), the number of dilated cristae, and the presence of autophagic vesicles without altering mitochondrial number or respiratory capacity. Additionally, lipid infusion suppressed peripheral glucose disposal (P = 0.004) and hepatic insulin sensitivity (P = 0.014). CONCLUSIONS These findings indicate that activation of mitochondrial fission and quality control occur early in the onset of insulin resistance in human skeletal muscle. Targeting mitochondrial dynamics and quality control represents a promising new pharmacological approach for treating insulin resistance and type 2 diabetes. CLINICAL TRIAL REGISTRATION NCT02697201, ClinicalTrials.gov.
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Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women.
Yoshino, M, Yoshino, J, Kayser, BD, Patti, GJ, Franczyk, MP, Mills, KF, Sindelar, M, Pietka, T, Patterson, BW, Imai, SI, et al
Science (New York, N.Y.). 2021;372(6547):1224-1229
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Nicotinamide adenine dinucleotide (NAD+) is a co-substrate for NAD+-consuming enzymes that are essential in the regulation of diverse biological processes. The aim of this study was to determine the effects of nicotinamide mononucleotide (NMN) supplementation on i) body composition, ii) skeletal muscle insulin sensitivity, and insulin signalling; and iii) muscle NAD+ content and global gene expression profile. This study is a 10-week, randomized, placebo-controlled, double-blind trial in postmenopausal women with prediabetes who were overweight or obese. Twenty-five postmenopausal women with prediabetes were randomised to the placebo group (n=12) or the NMN group (n=13). Results show that 10 weeks of NMN supplementation increases muscle insulin signalling and muscle insulin sensitivity in postmenopausal women with prediabetes who are overweight or obese. Authors conclude that the precise mechanism(s) responsible for these metabolic effects and the potential metabolic benefits of NMN supplementation in other patient populations remain to be explored.
Abstract
In rodents, obesity and aging impair nicotinamide adenine dinucleotide (NAD+) biosynthesis, which contributes to metabolic dysfunction. Nicotinamide mononucleotide (NMN) availability is a rate-limiting factor in mammalian NAD+ biosynthesis. We conducted a 10-week, randomized, placebo-controlled, double-blind trial to evaluate the effect of NMN supplementation on metabolic function in postmenopausal women with prediabetes who were overweight or obese. Insulin-stimulated glucose disposal, assessed by using the hyperinsulinemic-euglycemic clamp, and skeletal muscle insulin signaling [phosphorylation of protein kinase AKT and mechanistic target of rapamycin (mTOR)] increased after NMN supplementation but did not change after placebo treatment. NMN supplementation up-regulated the expression of platelet-derived growth factor receptor β and other genes related to muscle remodeling. These results demonstrate that NMN increases muscle insulin sensitivity, insulin signaling, and remodeling in women with prediabetes who are overweight or obese (clinicaltrial.gov NCT03151239).
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Effect of a Low-Fat Vegan Diet on Body Weight, Insulin Sensitivity, Postprandial Metabolism, and Intramyocellular and Hepatocellular Lipid Levels in Overweight Adults: A Randomized Clinical Trial.
Kahleova, H, Petersen, KF, Shulman, GI, Alwarith, J, Rembert, E, Tura, A, Hill, M, Holubkov, R, Barnard, ND
JAMA network open. 2020;3(11):e2025454
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Obesity is uncommon in individuals on a plant-based diet, possibly due to the high-fiber low fat nature of this style of eating and due to the fact that low levels of fat may increase metabolism levels. The aim of this randomised control trial of 244 people following a vegan diet was to assess the effects of a low-fat vegan diet on body weight, insulin resistance (IR), metabolism and lipid levels in the liver and muscle over 16 weeks. The results showed that individuals who followed the low-fat vegan diet as opposed to a normal vegan diet lost more weight, attributed to a loss of body fat and had decreased cholesterol levels. Measures of how the body balances blood sugars were improved and this was directly related to weight loss. The amount of energy needed to digest the food in the intervention diet was increased compared to the control group and this was involved in a relationship whereby as fat mass decreased, blood sugar balance improved, and metabolism increased. Liver lipids decreased in the intervention group, which was directly related to body weight loss and as liver lipids decreased, blood sugar balance increased. Muscle lipids were significantly decreased in the intervention group compared to the control group. It was shown that as fat mass decreased, muscle fat levels and blood sugar balance improved. It was concluded that the low-fat plant-based diet reduced body weight due to a reduced energy intake and increased body metabolism following eating. Blood sugar control was improved due to reduced fat levels in the muscles and liver. This study could be used by healthcare professionals to recommend a low-fat plant based diet to individuals who are overweight and/or who are showing signs of blood sugar imbalance.
Abstract
Importance: Excess body weight and insulin resistance lead to type 2 diabetes and other major health problems. There is an urgent need for dietary interventions to address these conditions. Objective: To measure the effects of a low-fat vegan diet on body weight, insulin resistance, postprandial metabolism, and intramyocellular and hepatocellular lipid levels in overweight adults. Design, Setting, and Participants: This 16-week randomized clinical trial was conducted between January 2017 and February 2019 in Washington, DC. Of 3115 people who responded to flyers in medical offices and newspaper and radio advertisements, 244 met the participation criteria (age 25 to 75 years; body mass index of 28 to 40) after having been screened by telephone. Interventions: Participants were randomized in a 1:1 ratio. The intervention group (n = 122) was asked to follow a low-fat vegan diet and the control group (n = 122) to make no diet changes for 16 weeks. Main Outcomes and Measures: At weeks 0 and 16, body weight was assessed using a calibrated scale. Body composition and visceral fat were measured by dual x-ray absorptiometry. Insulin resistance was assessed with the homeostasis model assessment index and the predicted insulin sensitivity index (PREDIM). Thermic effect of food was measured by indirect calorimetry over 3 hours after a standard liquid breakfast (720 kcal). In a subset of participants (n = 44), hepatocellular and intramyocellular lipids were quantified by proton magnetic resonance spectroscopy. Repeated measure analysis of variance was used for statistical analysis. Results: Among the 244 participants in the study, 211 (87%) were female, 117 (48%) were White, and the mean (SD) age was 54.4 (11.6) years. Over the 16 weeks, body weight decreased in the intervention group by 5.9 kg (95% CI, 5.0-6.7 kg; P < .001). Thermic effect of food increased in the intervention group by 14.1% (95% CI, 6.5-20.4; P < .001). The homeostasis model assessment index decreased (-1.3; 95% CI, -2.2 to -0.3; P < .001) and PREDIM increased (0.9; 95% CI, 0.5-1.2; P < .001) in the intervention group. Hepatocellular lipid levels decreased in the intervention group by 34.4%, from a mean (SD) of 3.2% (2.9%) to 2.4% (2.2%) (P = .002), and intramyocellular lipid levels decreased by 10.4%, from a mean (SD) of 1.6 (1.1) to 1.5 (1.0) (P = .03). None of these variables changed significantly in the control group over the 16 weeks. The change in PREDIM correlated negatively with the change in body weight (r = -0.43; P < .001). Changes in hepatocellular and intramyocellular lipid levels correlated with changes in insulin resistance (both r = 0.51; P = .01). Conclusions and Relevance: A low-fat plant-based dietary intervention reduces body weight by reducing energy intake and increasing postprandial metabolism. The changes are associated with reductions in hepatocellular and intramyocellular fat and increased insulin sensitivity. Trial Registration: ClinicalTrials.gov Identifier: NCT02939638.
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The Weight Optimization Revamping Lifestyle using the Dietary Guidelines (WORLD) Study: Sustained Weight Loss Over 12 Months.
Psota, TL, Tindall, AM, Lohse, B, Miller, PE, Petersen, KS, Kris-Etherton, PM
Obesity (Silver Spring, Md.). 2020;28(7):1235-1244
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Effective long-term weight loss strategies to reduce the risk of death and diseases associated with being obese or overweight are required, as restrictive programmes are difficult to sustain, and weight loss may be heavily influenced by behavioural factors. This randomised control trial of 101 premenopausal women with obesity or overweight aimed to compare a lower-fat and moderate-fat diets, both with nutrition education for 12 months. The results showed that both treatment groups lost weight. Both groups consumed the same amount of fat but increased their diet quality. Diet quality and greater attendance at nutritional education sessions were associated with greater weight loss. Cholesterol was significantly lower in both groups, but blood pressure remained unchanged. Interestingly there were a large number of women who did not complete the trial. It was concluded that irrespective of the amount of fat consumed, nutrition education can help to achieve sustained weight loss, improve diet quality and decrease heart disease risk for at least 12 months. This study could be used by healthcare professionals to understand that recommending fat-based targets for weight loss may be ineffective and the importance of emotional and behavioural support for individuals on a weight loss regime to improve their risk for heart disease.
Abstract
OBJECTIVE This study aimed to compare two energy-restricted, nutrient-dense diets at the upper or lower ends of the dietary fat recommendation range (lower fat [20% energy from fat] versus moderate fat [35%]) on weight loss using behavioral theory-based nutrition education. METHODS A total of 101 premenopausal women with overweight or obesity were randomized to an energy-restricted lower-fat or moderate-fat diet for 1 year. Interventions included 28 behavioral theory-based nutrition education sessions plus weekly exercise sessions. RESULTS Both treatment groups experienced weight loss (-5.0 kg for lower fat and -4.3 kg for moderate fat; P < 0.0001), but there was no difference in weight loss or fat intake between groups. Total and low-density lipoprotein cholesterol decreased (-3. 4 mg/dL and -3.8 mg/dL; P < 0.05), and high-density lipoprotein cholesterol increased (1.9 mg/dL; P < 0.05) in both groups at 12 months. Diet quality, assessed by the Healthy Eating Index, increased significantly at 4 months versus baseline (70.8 [0.9] vs. 77.8 [1.0]) and was maintained through 12 months. Higher Healthy Eating Index scores were associated with greater weight loss at 4 months (r = -0.2; P < 0.05). CONCLUSIONS In the context of a well-resourced, free-living weight-loss intervention, total fat intake did not change; however, theory-based nutrition education underpinned by food-based recommendations resulted in caloric deficits, improvements in diet quality, and weight loss that was sustained for 1 year.
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Insulin resistance drives hepatic de novo lipogenesis in nonalcoholic fatty liver disease.
Smith, GI, Shankaran, M, Yoshino, M, Schweitzer, GG, Chondronikola, M, Beals, JW, Okunade, AL, Patterson, BW, Nyangau, E, Field, T, et al
The Journal of clinical investigation. 2020;130(3):1453-1460
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Non-alcoholic fatty liver disease (NAFLD) is a common complication of obesity and is associated with multiorgan insulin resistance, dyslipidaemia and an increased risk of diabetes and coronary heart disease. The aims of this study were to (a) determine hepatic de novo lipogenesis (DNL) [the liver’s biochemical process of synthesising fatty acids] in 3 distinct cohorts, (b) determine the relationships among hepatic DNL and intrahepatic [within the liver] triglyceride (IHTG) content, and (c) determine the effect of moderate (10%) weight loss. This study is a cross-sectional study which included a total of 67 men and women (mean age: 39 ± 1 years; 14 men and 53 women). Results highlight the importance of DNL in the pathogenesis of hepatic steatosis [build up of fats in the liver] and suggest that increases in daily 24-hour plasma glucose and insulin concentrations are major drivers of increased DNL in individuals with obesity and NAFLD. Additionally, moderate (10%) weight loss caused a marked decrease in both hepatic DNL and IHTG content. Authors conclude that increases in circulating glucose and insulin promote hepatic DNL in individuals with NAFLD. Whereas an improvement in insulin sensitivity and a decrease in hepatic DNL, are potentially important contributors to the decline in IHTG content associated with moderate weight loss.
Abstract
BACKGROUNDAn increase in intrahepatic triglyceride (IHTG) is the hallmark feature of nonalcoholic fatty liver disease (NAFLD) and is decreased by weight loss. Hepatic de novo lipogenesis (DNL) contributes to steatosis in individuals with NAFLD. The physiological factors that stimulate hepatic DNL and the effect of weight loss on hepatic DNL are not clear.METHODSHepatic DNL, 24-hour integrated plasma insulin and glucose concentrations, and both liver and whole-body insulin sensitivity were determined in individuals who were lean (n = 14), obese with normal IHTG content (n = 26), or obese with NAFLD (n = 27). Hepatic DNL was assessed using the deuterated water method corrected for the potential confounding contribution of adipose tissue DNL. Liver and whole-body insulin sensitivity was assessed using the hyperinsulinemic-euglycemic clamp procedure in conjunction with glucose tracer infusion. Six subjects in the obese-NAFLD group were also evaluated before and after a diet-induced weight loss of 10%.RESULTSThe contribution of hepatic DNL to IHTG-palmitate was 11%, 19%, and 38% in the lean, obese, and obese-NAFLD groups, respectively. Hepatic DNL was inversely correlated with hepatic and whole-body insulin sensitivity, but directly correlated with 24-hour plasma glucose and insulin concentrations. Weight loss decreased IHTG content, in conjunction with a decrease in hepatic DNL and 24-hour plasma glucose and insulin concentrations.CONCLUSIONSThese data suggest hepatic DNL is an important regulator of IHTG content and that increases in circulating glucose and insulin stimulate hepatic DNL in individuals with NAFLD. Weight loss decreased IHTG content, at least in part, by decreasing hepatic DNL.TRIAL REGISTRATIONClinicalTrials.gov NCT02706262.FUNDINGThis study was supported by NIH grants DK56341 (Nutrition Obesity Research Center), DK20579 (Diabetes Research Center), DK52574 (Digestive Disease Research Center), and RR024992 (Clinical and Translational Science Award), and by grants from the Academy of Nutrition and Dietetics Foundation, the College of Natural Resources of UCB, and the Pershing Square Foundation.