-
1.
High-intensity interval training improves metabolic syndrome and body composition in outpatient cardiac rehabilitation patients with myocardial infarction.
Dun, Y, Thomas, RJ, Smith, JR, Medina-Inojosa, JR, Squires, RW, Bonikowske, AR, Huang, H, Liu, S, Olson, TP
Cardiovascular diabetology. 2019;18(1):104
-
-
-
Free full text
Plain language summary
Metabolic syndrome (MetS) is associated with an eightfold increase in the risk of myocardial infarction (MI), and MI patients who have MetS have an increased risk of other cardiovascular events and recurrent MI. Exercise can improve MetS and is also recommended for patients after MI for rehabilitation. The aim of this retrospective study was to examine the effect of supervised high intensity interval training (HIIT) on MetS and body composition in overweight patients with MI. Of 56 patients who took part in a multidisciplinary rehabilitation program, 42 had engaged in HIIT and 14 in moderate-intensity continuous training (MICT), both groups had 36 supervised sessions over 12 weeks. Compared to MICT, the HIIT group demonstrated greater reductions in MetS. Better improvements in the HIIT group were seen in waist circumference, fasting blood glucose, triglycerides, diastolic blood pressure, body fat and lean mass, compared to the MICT group. There were no significant differences between groups in changes in BMI, HDL cholesterol and systolic blood pressure. The authors concluded that their findings support the use of HIIT to improve MetS in MI patients
Abstract
BACKGROUND To examine the effect of high-intensity interval training (HIIT) on metabolic syndrome (MetS) and body composition in cardiac rehabilitation (CR) patients with myocardial infarction (MI). METHODS We retrospectively screened 174 consecutive patients with MetS enrolled in CR following MI between 2015 and 2018. We included 56 patients who completed 36 CR sessions and pre-post dual-energy X-ray absorptiometry. Of these patients, 42 engaged in HIIT and 14 in moderate-intensity continuous training (MICT). HIIT included 4-8 intervals of high-intensity (30-60 s at RPE 15-17 [Borg 6-20]) and low-intensity (1-5 min at RPE < 14), and MICT included 20-45 min of exercise at RPE 12-14. MetS and body composition variables were compared between MICT and HIIT groups. RESULTS Compared to MICT, HIIT demonstrated greater reductions in MetS (relative risk = 0.5, 95% CI 0.33-0.75, P < .001), MetS z-score (- 3.6 ± 2.9 vs. - 0.8 ± 3.8, P < .001) and improved MetS components: waist circumference (- 3 ± 5 vs. 1 ± 5 cm, P = .01), fasting blood glucose (- 25.8 ± 34.8 vs. - 3.9 ± 25.8 mg/dl, P < .001), triglycerides (- 67.8 ± 86.7 vs. - 10.4 ± 105.3 mg/dl, P < .001), and diastolic blood pressure (- 7 ± 11 vs. 0 ± 13 mmHg, P = .001). HIIT group demonstrated greater reductions in body fat mass (- 2.1 ± 2.1 vs. 0 ± 2.2 kg, P = .002), with increased body lean mass (0.9 ± 1.9 vs. - 0.9 ± 3.2 kg, P = .01) than the MICT. After matching for exercise energy expenditure, HIIT-induced improvements persisted for MetS z-score (P < .001), MetS components (P < .05), body fat mass (P = .002), body fat (P = .01), and lean mass (P = .03). CONCLUSIONS Our data suggest that, compared to MICT, supervised HIIT results in greater improvements in MetS and body composition in MI patients with MetS undergoing CR.
-
2.
Dietary fiber intake and glycemic control: coronary artery calcification in type 1 diabetes (CACTI) study.
Basu, A, Alman, AC, Snell-Bergeon, JK
Nutrition journal. 2019;18(1):23
-
-
-
Free full text
Plain language summary
The incidence of type 1 diabetes and cardiovascular disease, the major vascular complication of diabetes, have been increasing wordwide. The aim of the study is to identify the associations of dietary fibre with glycaemic control. The study is a cross-sectional longitudinal study which enrolled 1257 individuals in the cross-sectional analysis and a total of 990 participants were included in the longitudinal analysis. The participants had no known history of coronary heart disease. Results indicate an inverse association between total fibre intake and the average blood glucose levels for the last two to three months in both diabetic and nondiabetic participants. Authors conclude that their study provides some evidence on the role dietary fibre intake plays on glycaemic control, which is important in the management of type 1 diabetes in patients at high risk of cardiovascular disease.
Abstract
BACKGROUND Dietary fiber has been recommended for glucose control, and typically low intakes are observed in the general population. The role of fiber in glycemic control in reported literature is inconsistent and few reports are available in populations with type 1 diabetes (T1D). METHODS Using data from the Coronary Artery Calcification in Type 1 Diabetes (CACTI) study [n = 1257; T1D: n = 568; non-diabetic controls: n = 689] collected between March 2000 and April 2002, we examined cross-sectional (baseline) and longitudinal (six-year follow-up in 2006-2008) associations of dietary fiber and HbA1c. Participants completed a validated food frequency questionnaire, and a physical examination and fasting biochemical analyses (12 h fast) at baseline visit and at the year 6 visit. We used a linear regression model stratified by diabetes status, and adjusted for age, sex and total calories, and diabetes duration in the T1D group. We also examined correlations of dietary fiber with HbA1c. RESULTS Baseline dietary fiber intake and serum HbA1c in the T1D group were 16 g [median (IQ): 11-22 g) and 7.9 ± 1.3% mean (SD), respectively, and in the non-diabetic controls were 15 g [median (IQ): 11-21 g) and 5.4 ± 0.4%, respectively. Pearson partial correlation coefficients revealed a significant but weak inverse association of total dietary fiber with HbA1c when adjusted for age, sex, diabetes status and total calories (r = - 0.07, p = 0.01). In the adjusted linear regression model at baseline, total dietary fiber revealed a significant inverse association with HbA1c in the T1D group [β ± SE = - 0.32 ± 0.15, p = 0.034], as well as in the non-diabetic controls [- 0.10 ± 0.04, p = 0.009]. However, these results were attenuated after adjustment for dietary carbohydrates, fats and proteins, or for cholesterol and triglycerides. No such significance was observed at the year 6 follow-up, and with the HbA1c changes over 6 years. CONCLUSION Thus, at observed levels of intake, total dietary fiber reveals modest inverse associations with poor glycemic control. Future studies must further investigate the role of overall dietary quality adjusting for fiber-rich foods in T1D management.
-
3.
Fructose metabolism and metabolic disease.
Hannou, SA, Haslam, DE, McKeown, NM, Herman, MA
The Journal of clinical investigation. 2018;128(2):545-555
-
-
-
Free full text
-
Plain language summary
Sugar consumption is thought to be a contributing factor in the increase in diabetes and obesity and the associated risk of cardiovascular disease worldwide. Sucrose (table sugar) and high fructose corn syrup contain almost equal amounts of fructose and glucose and are commonly added to processed foods. Whilst long-term studies are lacking, some short-term intervention studies show that fructose can impair lipid metabolism and insulin sensitivity in humans. This article reviews the biochemistry and molecular genetics of fructose metabolism as well as potential mechanisms by which excessive fructose consumption contributes to cardiometabolic disease. Fructose absorption in the human intestine is saturable, and there is a large range in capacity to absorb fructose between individuals, and unabsorbed fructose may contribute to gastrointestinal symptoms including pain and bloating. Fructose concentrations in the blood can increase 10-fold after consumption, but are rapidly cleared, mostly by the liver, where it provides substrate for metabolic processes, but may also be involved in signalling functions. Fructose may enhance glucose uptake by the liver and storage as glycogen and lipids. It may also increase production of uric acid which is implicated with gout. Excessive fructose consumption affects lipid metabolism and may contribute to fat accumulation in the liver and increase circulating triglycerides, a risk factor for heart disease. In animal models it also induces increased insulin levels. Fructose is one of the sweetest sugars which may affect appetite and overeating. It may also induce addiction-like behaviours such as binging and dependence in part by stimulating dopaminergic pathways. It also appears to induce leptin resistance which further increases food intake and obesity.
Abstract
Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.
-
4.
Circulating bile acids in healthy adults respond differently to a dietary pattern characterized by whole grains, legumes and fruits and vegetables compared to a diet high in refined grains and added sugars: A randomized, controlled, crossover feeding study.
Ginos, BNR, Navarro, SL, Schwarz, Y, Gu, H, Wang, D, Randolph, TW, Shojaie, A, Hullar, MAJ, Lampe, PD, Kratz, M, et al
Metabolism: clinical and experimental. 2018;83:197-204
-
-
-
Free full text
-
Plain language summary
Bile acids are produced in the liver and are important for the absorption of fat and fat-soluble vitamins. About 95% of bile acids are reabsorbed. Circulating plasma bile acids can affect glucose metabolism and inflammation, and are thought to play a role in the development of metabolic syndrome. The aim of this study was to evaluate how plasma bile acid levels are influenced by a diet rich in whole grains, legumes, fruit and vegetables (low glycaemic load, GL) compared to a diet high in refined grains and sugar (high GL). The study evaluated data from a previous double-blind randomised, cross over feeding trial. 80 healthy adults had the low or high GL diet for four weeks, and after a four-week washout period, received the other diet for four weeks. Three specific plasma bile acids, which are thought to have a positive impact on glucose metabolism, were higher in the low GL group compared to the high GL group. Some individual plasma bile acids were positively associated with HOMA-IR (a measure of glucose metabolism/insulin resistance). There was no significant association between bile acid concentrations and C-reactive protein (a marker of inflammation). The authors conclude that the increase in certain bile acids on the low GL diet may be beneficial and that this effect may be to some extent mediated by the impact of the higher fibre content of the low GL diet on the gut microbial metabolism, which affects plasma bile acid levels.
Abstract
OBJECTIVE The effects of diets high in refined grains on biliary and colonic bile acids have been investigated extensively. However, the effects of diets high in whole versus refined grains on circulating bile acids, which can influence glucose homeostasis and inflammation through activation of farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (TGR5), have not been studied. MATERIALS AND METHODS We conducted a secondary analysis from a randomized controlled crossover feeding trial (NCT00622661) in 80 healthy adults (40 women/40 men, age 18-45 years) from the greater Seattle Area, half of which were normal weight (BMI 18.5-25.0 kg/m2) and half overweight to obese (BMI 28.0-39.9 kg/m2). Participants consumed two four-week controlled diets in randomized order: 1) a whole grain diet (WG diet), designed to be low in glycemic load (GL), high in whole grains, legumes, and fruits and vegetables, and 2) a refined grain diet (RG diet), designed to be high GL, high in refined grains and added sugars, separated by a four-week washout period. Quantitative targeted analysis of 55 bile acid species in fasting plasma was performed using liquid chromatography tandem mass spectrometry. Concentrations of glucose, insulin, and CRP were measured in fasting serum. Linear mixed models were used to test the effects of diet on bile acid concentrations, and determine the association between plasma bile acid concentrations and HOMA-IR and CRP. Benjamini-Hochberg false discovery rate (FDR) < 0.05 was used to control for multiple testing. RESULTS A total of 29 plasma bile acids were reliably detected and retained for analysis. Taurolithocholic acid (TLCA), taurocholic acid (TCA) and glycocholic acid (GCA) were statistically significantly higher after the WG compared to the RG diet (FDR < 0.05). There were no significant differences by BMI or sex. When evaluating the association of bile acids and HOMA-IR, GCA, taurochenodeoxycholic acid, ursodeoxycholic acid (UDCA), 5β‑cholanic acid‑3β,12α‑diol, 5‑cholanic acid‑3β‑ol, and glycodeoxycholic acid (GDCA) were statistically significantly positively associated with HOMA-IR individually, and as a group, total, 12α‑hydroxylated, primary and secondary bile acids were also significant (FDR < 0.05). When stratifying by BMI, chenodeoxycholic acid (CDCA), cholic acid (CA), UDCA, 5β-cholanic acid-3β, deoxycholic acid, and total, 12α-hydroxylated, primary and secondary bile acid groups were significantly positively associated with HOMA-IR among overweight to obese individuals (FDR < 0.05). When stratifying by sex, GCA, CDCA, TCA, CA, UDCA, GDCA, glycolithocholic acid (GLCA), total, primary, 12α‑hydroxylated, and glycine-conjugated bile acids were significantly associated with HOMA-IR among women, and CDCA, GDCA, and GLCA were significantly associated among men (FDR < 0.05). There were no significant associations between bile acids and CRP. CONCLUSIONS Diets with comparable macronutrient and energy composition, but differing in carbohydrate source, affected fasting plasma bile acids differently. Specifically, a diet characterized by whole grains, legumes, and fruits and vegetables compared to a diet high in refined grains and added sugars led to modest increases in concentrations of TLCA, TCA and GCA, ligands for FXR and TGR5, which may have beneficial effects on glucose homeostasis.
-
5.
A whole-grain diet reduces peripheral insulin resistance and improves glucose kinetics in obese adults: A randomized-controlled trial.
Malin, SK, Kullman, EL, Scelsi, AR, Haus, JM, Filion, J, Pagadala, MR, Godin, JP, Kochhar, S, Ross, AB, Kirwan, JP
Metabolism: clinical and experimental. 2018;82:111-117
-
-
-
Free full text
-
Plain language summary
Literature shows that dietary whole-grain intake is associated with a lower incidence of type 2 diabetes. The aim of the study was to investigate the association between a whole-grain diet and insulin resistance and glucose use in individuals at risk for type 2 diabetes. The study was a randomized, double-blind, controlled crossover trial involving fourteen middle-aged, obese adults at risk for diabetes. Randomisation was carried out prior to metabolic testing. Results indicate that whole-grain intake as part of a mixed-meal diet significantly improved post-prandial (after a meal) glucose metabolism in middle-aged obese adults. Furthermore, both whole-grain and refined-grain interventions induced about 3–6% weight and fat loss. Authors conclude that whole-grain intake effectively promotes glycaemic control by improving insulin action.
Abstract
BACKGROUND Whole-grain intake is associated with lower risk of type 2 diabetes but the mechanisms are unclear. PURPOSE We tested the hypothesis that a WG diet reduces insulin resistance and improves glucose use in individuals at risk for type 2 diabetes compared with an isocaloric-matched refined-grain diet. METHODS A double-blind, randomized, controlled, crossover trial of 14 moderately obese adults (Age, 38 ± 2 y; BMI, 34.0 ± 1.1 kg/m2). Insulin resistance and glucose metabolism was assessed using an oral glucose tolerance test combined with isotopic tracers of [6,6-2H2]-glucose and [U-13C]-glucose, and indirect calorimetry. Peripheral and hepatic insulin resistance was assessed as 1/(rate of disposal/insulin), and endogenous glucose rates of appearance (Ra) iAUC60-240 × insulin iAUC60-240, respectively. Both diets met ADA nutritional guidelines and contained either whole-grain (50 g per 1000 kcal) or equivalent refined-grain. All food was provided for 8 wk. with an 8-10 wk. washout period between diets. RESULTS Post-prandial glucose tolerance, peripheral insulin sensitivity, and metabolic flexibility (insulin-stimulated - fasting carbohydrate oxidation) improvements were greater after whole-grain compared to the refined-grain diet (P < 0.05). Compared to baseline, body fat (~2 kg) and hepatic Ra insulin resistance was reduced by both diets, while fasting glucose and exogenous glucose-meal were unchanged after both interventions. Changes in peripheral insulin resistance and metabolic flexibility correlated with improved glucose tolerance (P < 0.05). CONCLUSION Whole-grains reduced diabetes risk and the mechanisms appear to work through reduced post-prandial blood glucose and peripheral insulin resistance that were statistically linked to enhanced metabolic flexibility.
-
6.
Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis.
Manheimer, EW, van Zuuren, EJ, Fedorowicz, Z, Pijl, H
The American journal of clinical nutrition. 2015;102(4):922-32
-
-
-
Free full text
-
Plain language summary
Metabolic syndrome is a cluster of 5 risk factors, including waist circumference, blood pressure, and serum concentrations of glucose, triglycerides, and high-density lipoprotein (HDL) cholesterol in the fasting condition. These often occur in concert and predispose people to type 2 diabetes and cardiovascular disease. The aim of this study was to evaluate whether current evidence supports the idea that Paleolithic nutrition improves risk factors for chronic disease more than do other dietary interventions in people with one or more components of the metabolic syndrome. The study is a systematic review and meta-analysis of 4 randomized controlled trials that compared Paleolithic nutrition with any other dietary intervention in participants with one or more of the 5 components of the metabolic syndrome. Results indicate that Paleolithic nutrition resulted in greater short-term pooled improvements on each of the 5 components of metabolic syndrome than did currently recommended guideline-based control diets. However, the greater pooled improvements did not reach significance for 2 of the 5 components (i.e., HDL cholesterol and fasting blood sugar). Authors conclude that the available data warrant additional evaluations of the health benefits of Paleolithic nutrition.
Abstract
BACKGROUND Paleolithic nutrition, which has attracted substantial public attention lately because of its putative health benefits, differs radically from dietary patterns currently recommended in guidelines, particularly in terms of its recommendation to exclude grains, dairy, and nutritional products of industry. OBJECTIVE We evaluated whether a Paleolithic nutritional pattern improves risk factors for chronic disease more than do other dietary interventions. DESIGN We conducted a systematic review of randomized controlled trials (RCTs) that compared the Paleolithic nutritional pattern with any other dietary pattern in participants with one or more of the 5 components of metabolic syndrome. Two reviewers independently extracted study data and assessed risk of bias. Outcome data were extracted from the first measurement time point (≤6 mo). A random-effects model was used to estimate the average intervention effect. The quality of the evidence was rated with the use of the Grading of Recommendations Assessment, Development and Evaluation approach. RESULTS Four RCTs that involved 159 participants were included. The 4 control diets were based on distinct national nutrition guidelines but were broadly similar. Paleolithic nutrition resulted in greater short-term improvements than did the control diets (random-effects model) for waist circumference (mean difference: -2.38 cm; 95% CI: -4.73, -0.04 cm), triglycerides (-0.40 mmol/L; 95% CI: -0.76, -0.04 mmol/L), systolic blood pressure (-3.64 mm Hg; 95% CI: -7.36, 0.08 mm Hg), diastolic blood pressure (-2.48 mm Hg; 95% CI: -4.98, 0.02 mm Hg), HDL cholesterol (0.12 mmol/L; 95% CI: -0.03, 0.28 mmol/L), and fasting blood sugar (-0.16 mmol/L; 95% CI: -0.44, 0.11 mmol/L). The quality of the evidence for each of the 5 metabolic components was moderate. The home-delivery (n = 1) and dietary recommendation (n = 3) RCTs showed similar effects with the exception of greater improvements in triglycerides relative to the control with the home delivery. None of the RCTs evaluated an improvement in quality of life. CONCLUSIONS The Paleolithic diet resulted in greater short-term improvements in metabolic syndrome components than did guideline-based control diets. The available data warrant additional evaluations of the health benefits of Paleolithic nutrition. This systematic review was registered at PROSPERO (www.crd.york.ac.uk/PROSPERO) as CRD42014015119.
-
7.
Short sleep duration and dietary intake: epidemiologic evidence, mechanisms, and health implications.
Dashti, HS, Scheer, FA, Jacques, PF, Lamon-Fava, S, Ordovás, JM
Advances in nutrition (Bethesda, Md.). 2015;6(6):648-59
-
-
-
Free full text
-
Plain language summary
Short sleep duration is associated with various cardio-metabolic parameters that contribute to chronic disease. While the underlying mechanism is multifactorial, the link may be mediated through changes in dietary intake. This review provides an overview of the relationship between chronic short sleep duration and dietary intake. This review indicates that short sleep duration is associated with higher total caloric intake, higher fat intake and diets with relatively higher fat and lower protein composition. Further epidemiological studies are required to better establish the relationship between chronic short sleep and dietary patterns, and improvements in sleep should be an added factor in weight management programmes.
Abstract
Links between short sleep duration and obesity, type 2 diabetes, hypertension, and cardiovascular disease may be mediated through changes in dietary intake. This review provides an overview of recent epidemiologic studies on the relations between habitual short sleep duration and dietary intake in adults from 16 cross-sectional studies. The studies have observed consistent associations between short sleep duration and higher total energy intake and higher total fat intake, and limited evidence for lower fruit intake, and lower quality diets. Evidence also suggests that short sleepers may have irregular eating behavior deviating from the traditional 3 meals/d to fewer main meals and more frequent, smaller, energy-dense, and highly palatable snacks at night. Although the impact of short sleep duration on dietary intake tends to be small, if chronic, it may contribute to an increased risk of obesity and related chronic disease. Mechanisms mediating the associations between sleep duration and dietary intake are likely to be multifactorial and include differences in the appetite-related hormones leptin and ghrelin, hedonic pathways, extended hours for intake, and altered time of intake. Taking into account these epidemiologic relations and the evidence for causal relations between sleep loss and metabolism and cardiovascular function, health promotion strategies should emphasize improved sleep as an additional factor in health and weight management. Moreover, future sleep interventions in controlled studies and sleep extension trials in chronic short sleepers are imperative for establishing whether there is a causal relation between short sleep duration and changes in dietary intake.
-
8.
Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study.
Runchey, SS, Pollak, MN, Valsta, LM, Coronado, GD, Schwarz, Y, Breymeyer, KL, Wang, C, Wang, CY, Lampe, JW, Neuhouser, ML
European journal of clinical nutrition. 2012;66(10):1146-52
-
-
-
Free full text
-
Plain language summary
Dietary intervention studies have shown detrimental metabolic effects of high-glycaemic load diets. The glycaemic index (GI) is the numerical classification of a particular food’s blood glucose-raising effect. The aim of this study was to evaluate the effect of a high-glycaemic load diet on circulating levels of insulin-like growth factor-1 (IGF-1) [hormone] and insulin-like growth factor-binding protein 3 (IGFBP-3) [protein] compared to a low-glycaemic load diet. The study is a randomised controlled crossover study which enrolled 84 normal weight and overweight-obese healthy individuals. The study included two 28-day weight-maintaining high- and low-glycaemic load diets. Results indicate that consumption of a low-glycaemic load diet resulted in lower post-prandial [after a meal] insulin and glucose responses and modestly lower fasting IGF-1 and IGF-1/IGFBP-3 concentrations. However, there were no observable effects of glycaemic load on insulin resistance or glucose-adjusted post-prandial insulin responses in these healthy participants. Authors conclude that further intervention studies are required in order to weigh the impact of dietary glycaemic load on risk for chronic disease.
Abstract
BACKGROUND/OBJECTIVES The effect of a low glycemic load (GL) diet on insulin-like growth factor-1 (IGF-1) concentration is still unknown but may contribute to lower chronic disease risk. We aimed to assess the impact of GL on concentrations of IGF-1 and IGF-binding protein-3 (IGFBP-3). SUBJECTS/METHODS We conducted a randomized, controlled crossover feeding trial in 84 overweight obese and normal weight healthy individuals using two 28-day weight-maintaining high- and low-GL diets. Measures were fasting and post-prandial concentrations of insulin, glucose, IGF-1 and IGFBP-3. In all 80 participants completed the study and 20 participants completed post-prandial testing by consuming a test breakfast at the end of each feeding period. We used paired t-tests for diet component and linear mixed models for biomarker analyses. RESULTS The 28-day low-GL diet led to 4% lower fasting concentrations of IGF-1 (10.6 ng/ml, P=0.04) and a 4% lower ratio of IGF-1/IGFBP-3 (0.24, P=0.01) compared with the high-GL diet. The low-GL test breakfast led to 43% and 27% lower mean post-prandial glucose and insulin responses, respectively; mean incremental areas under the curve for glucose and insulin, respectively, were 64.3±21.8 (mmol/l/240 min; P<0.01) and 2253±539 (μU/ml/240 min; P<0.01) lower following the low- compared with the high-GL test meal. There was no effect of GL on mean homeostasis model assessment for insulin resistance or on mean integrated post-prandial concentrations of glucose-adjusted insulin, IGF-1 or IGFBP-3. We did not observe modification of the dietary effect by adiposity. CONCLUSIONS Low-GL diets resulted in 43% and 27% lower post-prandial responses of glucose and insulin, respectively, and modestly lower fasting IGF-1 concentrations. Further intervention studies are needed to weigh the impact of dietary GL on risk for chronic disease.
-
9.
Effects of dietary composition on energy expenditure during weight-loss maintenance.
Ebbeling, CB, Swain, JF, Feldman, HA, Wong, WW, Hachey, DL, Garcia-Lago, E, Ludwig, DS
JAMA. 2012;307(24):2627-34
-
-
-
Free full text
-
Plain language summary
Many diets can produce weight loss over the short term, but most people struggle to maintain this loss over the long term. One explanation is that weight loss results in biological effects, such as a decline in energy expenditure and an increase in hunger, that promote weight regain. The aim of the study was to examine the effects of three different diets on energy expenditure, hormones (including leptin, insulin, cortisol and thyroid hormones) and metabolic indicators following a 10-15% weight loss. The three diets differed widely in macronutrient composition and were: low-fat/high glycaemic load (60% energy from carbohydrates, 20%, 20% protein) LF; low glycaemic index (40%-40%-20%) LGI; and very low carbohydrate/low glycaemic load (10%-60%-30%) VLC. Participants were assigned to one of the three diets for four weeks. Participants on the VLC diet had a resting energy expenditure (REE) of 67kcal/day greater than the LF diet, as well as a total energy expenditure (TEE) of 300kcal/day greater. The physiological basis for these differences is unclear. Although the VLC diet produced the greatest improvements in most metabolic syndrome markers, it also resulted in increased cortisol and inflammation markers. These could be deleterious to health in the long term.
Abstract
CONTEXT Reduced energy expenditure following weight loss is thought to contribute to weight gain. However, the effect of dietary composition on energy expenditure during weight-loss maintenance has not been studied. OBJECTIVE To examine the effects of 3 diets differing widely in macronutrient composition and glycemic load on energy expenditure following weight loss. DESIGN, SETTING, AND PARTICIPANTS A controlled 3-way crossover design involving 21 overweight and obese young adults conducted at Children's Hospital Boston and Brigham and Women's Hospital, Boston, Massachusetts, between June 16, 2006, and June 21, 2010, with recruitment by newspaper advertisements and postings. INTERVENTION After achieving 10% to 15% weight loss while consuming a run-in diet, participants consumed an isocaloric low-fat diet (60% of energy from carbohydrate, 20% from fat, 20% from protein; high glycemic load), low-glycemic index diet (40% from carbohydrate, 40% from fat, and 20% from protein; moderate glycemic load), and very low-carbohydrate diet (10% from carbohydrate, 60% from fat, and 30% from protein; low glycemic load) in random order, each for 4 weeks. MAIN OUTCOME MEASURES Primary outcome was resting energy expenditure (REE), with secondary outcomes of total energy expenditure (TEE), hormone levels, and metabolic syndrome components. RESULTS Compared with the pre-weight-loss baseline, the decrease in REE was greatest with the low-fat diet (mean [95% CI], -205 [-265 to -144] kcal/d), intermediate with the low-glycemic index diet (-166 [-227 to -106] kcal/d), and least with the very low-carbohydrate diet (-138 [-198 to -77] kcal/d; overall P = .03; P for trend by glycemic load = .009). The decrease in TEE showed a similar pattern (mean [95% CI], -423 [-606 to -239] kcal/d; -297 [-479 to -115] kcal/d; and -97 [-281 to 86] kcal/d, respectively; overall P = .003; P for trend by glycemic load < .001). Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P < .001; 24-hour urinary cortisol, P = .005; indexes of peripheral [P = .02] and hepatic [P = .03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P < .001; non-HDL cholesterol, P < .001; triglycerides, P < .001; plasminogen activator inhibitor 1, P for trend = .04; and C-reactive protein, P for trend = .05), but no consistent favorable pattern emerged. CONCLUSION Among overweight and obese young adults compared with pre-weight-loss energy expenditure, isocaloric feeding following 10% to 15% weight loss resulted in decreases in REE and TEE that were greatest with the low-fat diet, intermediate with the low-glycemic index diet, and least with the very low-carbohydrate diet. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00315354.
-
10.
Hyperinsulinemia leads to uncoupled insulin regulation of the GLUT4 glucose transporter and the FoxO1 transcription factor.
Gonzalez, E, Flier, E, Molle, D, Accili, D, McGraw, TE
Proceedings of the National Academy of Sciences of the United States of America. 2011;108(25):10162-7
-
-
-
Free full text
-
Plain language summary
Insulin resistance develops following extended periods of high insulin production, making cells unresponsive to its actions, however not all insulin functions are equally affected. Patients with Type 2 diabetes have impaired insulin regulation of glucose with increased fat storage in the liver. This results in a combination of raised insulin, glucose and triglycerides in the blood (hyperinsulinemia, hyperglycaemia, and hypertriglyceridemia), which affect health outcomes. Studies have shown that 'selective insulin resistance' occurs in the liver, however the molecular mechanisms by which this occurs are not known. It is also not known whether this is liver-specific or occurs in other insulin responsive tissues in the body. This in-vitro (cell culture) study found that high levels of insulin disturbs the PI3-kinase/Akt signalling pathway resulting in selective insulin resistance in fat cells (adipocytes), whilst expression of FoxO1 transcription factor (which controls lipid metabolism) is maintained. These changes are the result of inherent differences in insulin sensitivity of GLUT4 translocation and FoxO1 nuclear exclusion. The authors conclude that in a model of chronic hyperinsulinemia, fat cells develop a state of selective insulin resistance. Uncoupled insulin action, a phenomenon first described in the insulin-resistant liver, might be a general feature of insulin-resistant tissues consequent to deregulation of PI3-kinase/Akt signalling.
Abstract
Insulin resistance is a component of the metabolic syndrome and Type 2 diabetes. It has been recently shown that in liver insulin resistance is not complete. This so-called selective insulin resistance is characterized by defective insulin inhibition of hepatic glucose output while insulin-induced lipogenesis is maintained. How this occurs and whether uncoupled insulin action develops in other tissues is unknown. Here we show in a model of chronic hyperinsulinemia that adipocytes develop selective insulin resistance in which translocation of the GLUT4 glucose transporter to the cell surface is blunted yet nuclear exclusion of the FoxO1 transcription factor is preserved, rendering uncoupled insulin-controlled carbohydrate and lipid metabolisms. We found that in adipocytes FoxO1 nuclear exclusion has a lower half-maximal insulin dose than GLUT4 translocation, and it is because of this inherent greater sensitivity that control of FoxO1 by physiological insulin concentrations is maintained in adipocytes with compromised insulin signaling. Pharmacological and genetic interventions revealed that insulin regulates GLUT4 and FoxO1 through the PI3-kinase isoform p110α, although FoxO1 showed higher sensitivity to p110α activity than GLUT4. Transient down-regulation and overexpression of Akt isoforms in adipocytes demonstrated that insulin-activated PI3-kinase signals to GLUT4 primarily through Akt2 kinase, whereas Akt1 and Akt2 signal to FoxO1. We propose that the lower threshold of insulin activity for FoxO1's nuclear exclusion is in part due to its regulation by both Akt isoforms. Identification of uncoupled insulin action in adipocytes suggests this condition might be a general phenomenon of insulin target tissues contributing to insulin resistance's pathophysiology.