scholarly journals Differential Effects of One Meal per Day in the Evening on Metabolic Health and Physical Performance in Lean Individuals

2022 ◽  
Vol 12 ◽  
Author(s):  
Emma C. E. Meessen ◽  
Håvard Andresen ◽  
Thomas van Barneveld ◽  
Anne van Riel ◽  
Egil I. Johansen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Physical Performance ◽  
Fat Mass ◽  
Metabolic Health ◽  
Point Of View ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Total Body Mass ◽  
Single Meal

Background: Generally, food intake occurs in a three-meal per 24 h fashion with in-between meal snacking. As such, most humans spend more than ∼ 12–16 h per day in the postprandial state. It may be reasoned from an evolutionary point of view, that the human body is physiologically habituated to less frequent meals. Metabolic flexibility (i.e., reciprocal changes in carbohydrate and fatty acid oxidation) is a characteristic of metabolic health and is reduced by semi-continuous feeding. The effects of time-restricted feeding (TRF) on metabolic parameters and physical performance in humans are equivocal.Methods: To investigate the effect of TRF on metabolism and physical performance in free-living healthy lean individuals, we compared the effects of eucaloric feeding provided by a single meal (22/2) vs. three meals per day in a randomized crossover study. We included 13 participants of which 11 (5 males/6 females) completed the study: age 31.0 ± 1.7 years, BMI 24.0 ± 0.6 kg/m2 and fat mass (%) 24.0 ± 0.6 (mean ± SEM). Participants consumed all the calories needed for a stable weight in either three meals (breakfast, lunch and dinner) or one meal per day between 17:00 and 19:00 for 11 days per study period.Results: Eucaloric meal reduction to a single meal per day lowered total body mass (3 meals/day –0.5 ± 0.3 vs. 1 meal/day –1.4 ± 0.3 kg, p = 0.03), fat mass (3 meals/day –0.1 ± 0.2 vs. 1 meal/day –0.7 ± 0.2, p = 0.049) and increased exercise fatty acid oxidation (p < 0.001) without impairment of aerobic capacity or strength (p > 0.05). Furthermore, we found lower plasma glucose concentrations during the second half of the day during the one meal per day intervention (p < 0.05).Conclusion: A single meal per day in the evening lowers body weight and adapts metabolic flexibility during exercise via increased fat oxidation whereas physical performance was not affected.

scholarly journals Assessment of myocardial metabolic flexibility and work efficiency in human type 2 diabetes using 16-[18F]fluoro-4-thiapalmitate, a novel PET fatty acid tracer

2016 ◽  
Vol 310 (6) ◽  
pp. E452-E460 ◽  
Author(s):  
K. J. Mather ◽  
G. D. Hutchins ◽  
K. Perry ◽  
W. Territo ◽  
R. Chisholm ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Work Efficiency ◽  
Myocardial Fatty Acid ◽  
Fuel Selection

Altered myocardial fuel selection likely underlies cardiac disease risk in diabetes, affecting oxygen demand and myocardial metabolic flexibility. We investigated myocardial fuel selection and metabolic flexibility in human type 2 diabetes mellitus (T2DM), using positron emission tomography to measure rates of myocardial fatty acid oxidation {16-[18F]fluoro-4-thia-palmitate (FTP)} and myocardial perfusion and total oxidation ([11C]acetate). Participants underwent paired studies under fasting conditions, comparing 3-h insulin + glucose euglycemic clamp conditions (120 mU·m−2·min−1) to 3-h saline infusion. Lean controls ( n = 10) were compared with glycemically controlled volunteers with T2DM ( n = 8). Insulin augmented heart rate, blood pressure, and stroke index in both groups (all P < 0.01) and significantly increased myocardial oxygen consumption ( P = 0.04) and perfusion ( P = 0.01) in both groups. Insulin suppressed available nonesterified fatty acids ( P < 0.0001), but fatty acid concentrations were higher in T2DM under both conditions ( P < 0.001). Insulin-induced suppression of fatty acid oxidation was seen in both groups ( P < 0.0001). However, fatty acid oxidation rates were higher under both conditions in T2DM ( P = 0.003). Myocardial work efficiency was lower in T2DM ( P = 0.006) and decreased in both groups with the insulin-induced increase in work and shift in fuel utilization ( P = 0.01). Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. This is accompanied by reduced work efficiency, possibly due to greater oxygen consumption with fatty acid metabolism. These observations suggest that improved fatty acid suppression, or reductions in myocardial fatty acid uptake and retention, could be therapeutic targets to improve myocardial ischemia tolerance in T2DM.

scholarly journals ADCK2 Haploinsufficiency Reduces Mitochondrial Lipid Oxidation and Causes Myopathy Associated with CoQ Deficiency

2019 ◽  
Vol 8 (9) ◽  
pp. 1374 ◽  
Author(s):  
Vázquez-Fonseca ◽  
Schaefer ◽  
Navas-Enamorado ◽  
Santos-Ocaña ◽  
Hernández-Camacho ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Mouse Model ◽  
Fatty Acid Oxidation ◽  
Physical Performance ◽  
Liver Dysfunction ◽  
Mitochondrial Myopathy ◽  
Integrated Analysis ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid

Fatty acids and glucose are the main bioenergetic substrates in mammals. Impairment of mitochondrial fatty acid oxidation causes mitochondrial myopathy leading to decreased physical performance. Here, we report that haploinsufficiency of ADCK2, a member of the aarF domain-containing mitochondrial protein kinase family, in human is associated with liver dysfunction and severe mitochondrial myopathy with lipid droplets in skeletal muscle. In order to better understand the etiology of this rare disorder, we generated a heterozygous Adck2 knockout mouse model to perform in vivo and cellular studies using integrated analysis of physiological and omics data (transcriptomics–metabolomics). The data showed that Adck2+/− mice exhibited impaired fatty acid oxidation, liver dysfunction, and mitochondrial myopathy in skeletal muscle resulting in lower physical performance. Significant decrease in Coenzyme Q (CoQ) biosynthesis was observed and supplementation with CoQ partially rescued the phenotype both in the human subject and mouse model. These results indicate that ADCK2 is involved in organismal fatty acid metabolism and in CoQ biosynthesis in skeletal muscle. We propose that patients with isolated myopathies and myopathies involving lipid accumulation be tested for possible ADCK2 defect as they are likely to be responsive to CoQ supplementation.

Excess body fat in men decreases plasma fatty acid availability and oxidation during endurance exercise

2004 ◽  
Vol 286 (3) ◽  
pp. E354-E362 ◽  
Author(s):  
Bettina Mittendorfer ◽  
David A. Fields ◽  
Samuel Klein
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Fat Mass ◽  
Total Fatty Acid ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Plasma Fatty Acids ◽  
Exercise Induced

The effect of relative body fat mass on exercise-induced stimulation of lipolysis and fatty acid oxidation was evaluated in 15 untrained men (5 lean, 5 overweight, and 5 obese with body mass indexes of 21 ± 1, 27 ± 1, and 34 ± 1 kg/m2, respectively, and %body fat ranging from 12 to 32%). Palmitate and glycerol kinetics and substrate oxidation were assessed during 90 min of cycling at 50% peak aerobic capacity (V̇o2 peak) by use of stable isotope-labeled tracer infusion and indirect calorimetry. An inverse relationship was found between %body fat and exercise-induced increase in glycerol appearance rate relative to fat mass ( r2 = 0.74; P < 0.01). The increase in total fatty acid uptake during exercise [(μmol/kg fat-free mass) × 90 min] was ∼50% smaller in obese (181 ± 70; P < 0.05) and ∼35% smaller in overweight (230 ± 71; P < 0.05) than in lean (354 ± 34) men. The percentage of total fatty acid oxidation derived from systemic plasma fatty acids decreased with increasing body fat, from 49 ± 3% in lean to 39 ± 4% in obese men ( P < 0.05); conversely, the percentage of nonsystemic fatty acids, presumably derived from intramuscular and possibly plasma triglycerides, increased with increasing body fat ( P < 0.05). We conclude that the lipolytic response to exercise decreases with increasing adiposity. The blunted increase in lipolytic rate in overweight and obese men compared with lean men limits the availability of plasma fatty acids as a fuel during exercise. However, the rate of total fat oxidation was similar in all groups because of a compensatory increase in the oxidation of nonsystemic fatty acids.

SGLT2 selective inhibitor ipragliflozin reduces body fat mass by increasing fatty acid oxidation in high-fat diet-induced obese rats

2014 ◽  
Vol 727 ◽  
pp. 66-74 ◽  
Author(s):  
Masanori Yokono ◽  
Toshiyuki Takasu ◽  
Yuka Hayashizaki ◽  
Keisuke Mitsuoka ◽  
Rumi Kihara ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Fat Mass ◽  
High Fat Diet ◽  
Selective Inhibitor ◽  
Acid Oxidation ◽  
Body Fat Mass ◽  
High Fat ◽  
Obese Rats

scholarly journals Logical modelling reveals the PDC-PDK interaction as the regulatory switch driving metabolic flexibility at the cellular level

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Samar HK Tareen ◽  
Martina Kutmon ◽  
Ilja CW Arts ◽  
Theo M de Kok ◽  
Chris T Evelo ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Pyruvate Dehydrogenase ◽  
Tricarboxylic Acid Cycle ◽  
Pyruvate Dehydrogenase Complex ◽  
Tricarboxylic Acid ◽  
Cellular Level ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Acid Cycle

Abstract Background Metabolic flexibility is the ability of an organism to switch between substrates for energy metabolism, in response to the changing nutritional state and needs of the organism. On the cellular level, metabolic flexibility revolves around the tricarboxylic acid cycle by switching acetyl coenzyme A production from glucose to fatty acids and vice versa. In this study, we modelled cellular metabolic flexibility by constructing a logical model connecting glycolysis, fatty acid oxidation, fatty acid synthesis and the tricarboxylic acid cycle, and then using network analysis to study the behaviours of the model. Results We observed that the substrate switching usually occurs through the inhibition of pyruvate dehydrogenase complex (PDC) by pyruvate dehydrogenase kinases (PDK), which moves the metabolism from glycolysis to fatty acid oxidation. Furthermore, we were able to verify four different regulatory models of PDK to contain known biological observations, leading to the biological plausibility of all four models across different cells and conditions. Conclusion These results suggest that the cellular metabolic flexibility depends upon the PDC-PDK regulatory interaction as a key regulatory switch for changing metabolic substrates.

Muscle-derived expression of the chemokine CXCL1 attenuates diet-induced obesity and improves fatty acid oxidation in the muscle

2012 ◽  
Vol 302 (7) ◽  
pp. E831-E840 ◽  
Author(s):  
Line Pedersen ◽  
Caroline Holkmann Olsen ◽  
Bente Klarlund Pedersen ◽  
Pernille Hojman
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fat Mass ◽  
Subcutaneous Fat ◽  
Metabolic Effects ◽  
Acid Oxidation ◽  
High Fat ◽  
Physiological Range ◽  
Diet Induced Obesity

Serum levels and muscle expression of the chemokine CXCL1 increase markedly in response to exercise in mice. Because several studies have established muscle-derived factors as important contributors of metabolic effects of exercise, this study aimed at investigating the effect of increased expression of muscle-derived CXCL1 on systemic and intramuscular metabolic parameters, with focus on fatty acid oxidation and oxidative metabolism in skeletal muscle. By overexpression of CXCL1 in the tibialis cranialis muscle in mice, significant elevations in muscle and serum CXCL1 within a physiological range were obtained. At 3 mo of high-fat feeding, visceral and subcutaneous fat mass were 32.4 ( P < 0.01) and 22.4% ( P < 0.05) lower, respectively, in CXCL1-overexpressing mice compared with control mice. Also, chow-fed CXCL-transfected mice had 35.4% ( P < 0.05) lower visceral fat mass and 33.4% ( P < 0.05) lower subcutaneous fat mass compared with chow-fed control mice. These reductions in accumulation of adipose tissue were accompanied by improved glucose tolerance and insulin sensitivity. Furthermore, in CXCL1-transfected muscles, muscular ex vivo fatty acid oxidation was significantly enhanced compared with control muscles (chow fed: 2.2-fold, P < 0.05; high-fat fed: 2-fold, P < 0.05) and also showed increased expression levels of major fatty acid oxidation genes (CD36, CPT I, and HADH). Finally, CXCL1 expression was associated with increased muscle mRNA expression of VEGF and CD31, suggesting a role for CXCL1 in muscle angiogenesis. In conclusion, our data show that overexpression of CXCL1 within a physiological range attenuates diet-induced obesity, likely mediated through a CXCL1-induced improvement of fatty acid oxidation and oxidative capacity in skeletal muscle tissue.

Impairment of fat oxidation under high- vs. low-glycemic index diet occurs before the development of an obese phenotype

2010 ◽  
Vol 298 (2) ◽  
pp. E287-E295 ◽  
Author(s):  
F. Isken ◽  
S. Klaus ◽  
K. J. Petzke ◽  
C. Loddenkemper ◽  
A. F. H. Pfeiffer ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Body Fat ◽  
Fat Mass ◽  
Liver Fat ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Body Fat Mass ◽  
Short Term ◽  
Low Glycemic Index

Exposure to high vs. low glycemic index (GI) diets increases fat mass and insulin resistance in obesity-prone C57BL/6J mice. However, the longer-term effects and potentially involved mechanisms are largely unknown. We exposed four groups of male C57BL/6J mice ( n = 10 per group) to long-term (20 wk) or short-term (6 wk) isoenergetic and macronutrient matched diets only differing in starch type and as such GI. Body composition, liver fat, molecular factors of lipid metabolism, and markers of insulin sensitivity and metabolic flexibility were investigated in all four groups of mice. Mice fed the high GI diet showed a rapid-onset (from week 5) marked increase in body fat mass and liver fat, a gene expression profile in liver consistent with elevated lipogenesis, and, after long-term exposure, significantly reduced glucose clearance following a glucose load. The long-term high-GI diet also led to a delayed switch to both carbohydrate and fat oxidation in the postprandial state, indicating reduced metabolic flexibility. In contrast, no difference in carbohydrate oxidation was observed after short-term high- vs. low-GI exposure. However, fatty acid oxidation was significantly blunted as early as 3 wk after beginning of the high-GI intervention, at a time where most measured phenotypic markers including body fat mass were comparable between groups. Thus long-term high-GI feeding resulted in an obese, insulin-resistant, and metabolically inflexible phenotype in obesity-prone C57BL/6J mice. Early onset and significantly impaired fatty acid oxidation preceded these changes, thereby indicating a potentially causal involvement.

scholarly journals ADCK2 Haploinsufficiency Reduces Mitochondrial Lipid Oxidation and Causes Myopathy Associated with CoQ Deficiency

2019 ◽  
Author(s):  
Luis Vázquez-Fonseca ◽  
Jochen Schäfer ◽  
Ignacio Navas-Enamorado ◽  
Carlos Santos-Ocaña ◽  
Juan D. Hernández-Camacho ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Mouse Model ◽  
Fatty Acid Oxidation ◽  
Physical Performance ◽  
Liver Dysfunction ◽  
Mitochondrial Myopathy ◽  
Integrated Analysis ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid

Fatty acids and glucose are the main bioenergetic substrates in mammals that are alternatively used during the transition between fasting and feeding. Impairment of mitochondrial fatty acid oxidation causes mitochondrial myopathy leading to decreased physical performance. Here, we report that haploinsufficiency of ADCK2, a member of the aarF domain-containing mitochondrial protein kinase family, in human is associated with liver dysfunction and severe mitochondrial myopathy with lipid droplets in skeletal muscle. In order to better understand the etiology of this rare disorder, we generated a heterozygous Adck2 knockout mouse model to perform in vivo and cellular studies using integrated analysis of physiological and omics data (transcriptomics-metabolomics). The data show that Aldh2+/- mice exhibits impaired fatty acid oxidation, liver dysfunction, and mitochondrial myopathy in skeletal muscle resulting in lower physical performance. Significant decrease in CoQ biosynthesis was observed and supplementation with CoQ partially rescued the phenotype both in the human subject and mouse model. These results indicate that ADCK2 is involved in organismal fatty acid metabolism and in CoQ biosynthesis in skeletal muscle. We propose that patients with isolated myopathies and myopathies involving lipid accumulation be tested for possible ADCK2 defect as they are likely to be responsive to CoQ supplementation.

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