Increased Fat Oxidation Research Articles

Impact of Exercise-Nutritional State Interactions in Patients with Type 2 Diabetes.

This study examines the role of nutritional status during exercise training in patients with type 2 diabetes mellitus by investigating the effect of endurance-type exercise training in the fasted versus the fed state on clinical outcome measures, glycemic control, and skeletal muscle characteristics in male type 2 diabetes patients. Twenty-five male patients (glycated hemoglobin (HbA1c), 57 ± 3 mmol·mol (7.4% ± 0.3%)) participated in a randomized 12-wk supervised endurance-type exercise intervention, with exercise being performed in an overnight-fasted state (n = 13) or after consuming breakfast (n = 12). Patients were evaluated for glycemic control, blood lipid profiles, body composition and physical fitness, and skeletal muscle gene expression. Exercise training was well tolerated without any incident of hypoglycemia. Exercise training significantly decreased whole-body fat mass (-1.6 kg) and increased high-density lipoprotein concentrations (+2 mg·dL), physical fitness (+1.7 mL·min·kg), and fat oxidation during exercise in both groups (PTIME < 0.05), with no between-group differences (PTIME × GROUP > 0.05). HbA1c concentrations significantly decreased after exercise training (PTIME < 0.001), with a significant greater reduction after consuming breakfast (-0.30% ± 0.06%) compared with fasted state (-0.08% ± 0.06%; mean difference, 0.21%; PTIME × GROUP = 0.016). No interaction effects were observed for skeletal muscle genes related to lipid metabolism or oxidative capacity. Endurance-type exercise training in the fasted or fed state do not differ in their efficacy to reduce fat mass, increase fat oxidation capacity, and increase cardiorespiratory fitness and high-density lipoprotein concentrations or their risk of hypoglycemia in male patients with type 2 diabetes. HbA1c seems to be improved more with exercise performed in the postprandial compared with the postabsorptive state.

The In Vivo Net Energy Content of Resistant Starch and Its Effect on Macronutrient Oxidation in Healthy Adults.

The in vivo net energy content of resistant starch (RS) has not been measured in humans so it has not been possible to account for the contribution of RS to dietary energy intake. We aimed to determine the in vivo net energy content of RS and examine its effect on macronutrient oxidation. This was a randomized, double-blind cross-over study. Eighteen healthy adults spent 24 h in a whole room indirect calorimeter to measure total energy expenditure (TEE), substrate oxidation, and postprandial metabolites in response to three diets: 1) digestible starch (DS), 2) RS (33% dietary fiber; RS), or 3) RS with high fiber (RSF, 56% fiber). The in vivo net energy content of RS and RSF are 2.74 ± 0.41 and 3.16 ± 0.27 kcal/g, respectively. There was no difference in TEE or protein oxidation between DS, RS, and RSF. However, RS and RSF consumption caused a 32% increase in fat oxidation (p = 0.04) with a concomitant 18% decrease in carbohydrate oxidation (p = 0.03) versus DS. Insulin responses were unaltered after breakfast but lower in RS and RSF after lunch, at equivalent glucose concentrations, indicating improved insulin sensitivity. The average in vivo net energy content of RS is 2.95 kcal/g, regardless of dietary fiber content. RS and RSF consumption increase fat and decrease carbohydrate oxidation with postprandial insulin responses lowered after lunch, suggesting improved insulin sensitivity at subsequent meals.

Beneficial effects of running and milk protein supplements on Sirtuins and risk factors of metabolic disorders in rats with low aerobic capacity

BackgroundPhysical activity and dietary intake of dairy products are associated with improved metabolic health. Dairy products are rich with branched chain amino acids that are essential for energy production. To gain insight into the mechanisms underlying the benefit of the sub-chronic effects of running and intake of milk protein supplements, we studied Low Capacity Runner rats (LCR), a rodent exercise model with risk for metabolic disorders. We especially focused on the role of Sirtuins, energy level dependent proteins that affect many cellular metabolic processes. MethodsForty-seven adult LCR female rats sedentary or running voluntarily in wheels were fed normal chow and given supplements of either whey or milk protein drink (PD)-supplemented water, or water only for 21 weeks. Physiological responses were measured in vivo. Blood lipids were determined from serum. Mitochondrial markers and Sirtuins (Sirt1-7) including downstream targets were measured in plantaris muscle by western blotting. ResultsFor the first 10 weeks whey-drinking rats ran about 50% less compared to other groups; still, in all runners glucose tolerance improved and triglycerides decreased. Generally, running induced a ∼six-fold increase in running capacity and a ∼8% decrease in % body fat. Together with running, protein supplements increased the relative lean mass of the total body weight by ∼11%. In comparison with sedentary controls, running and whey increased HDL (21%) and whey, with or without running, lowered LDL (−34%). Running increased mitochondrial biogenesis and Sirtuins 3 and 4. When combined with exercise, both whey and milk protein drink induced about a 4-fold increase in Sirt3, compared to runners drinking water only, and about a 2-fold increase compared to the respective sedentary group. Protein supplements, with or without running, enhanced the phosphorylation level of the acetyl-coA-carboxylase, suggesting increased fat oxidation. Both supplemented diets increased Sirt5 and Sirt7 without an additional effect from exercise. Running diminished and PD supplement increased Sirt6. ConclusionWe demonstrate in rats new sub-chronic effects of milk proteins on metabolism that involve Sirtuins and their downstream targets in skeletal muscle. The results show that running and milk proteins act on reducing the risk factors of metabolic disorders and suggest that the underlying mechanisms may involve Sirtuins. Notably, we found that milk protein supplements have some favorable effects on metabolism even without running.

Cafestol increases fat oxidation and energy expenditure in Caenorhabditis elegans via DAF-12-dependent pathway

Cafestol, a coffee diterpene, is a known agonist of farnesoid X receptors (FXR), which are involved in cholesterol homeostasis. FXR plays critical roles in other lipid metabolic pathways, including fat oxidation; however, little is known about cafestol’s effects on fatty acid metabolism. Thus, the goal was to investigate cafestol’s effects on fatty acid metabolism using Caenorhabditis elegans. Cafestol at 60 µM reduced fat accumulation and increased locomotor activity (an indicator of energy expenditure) by 20% and 38%, respectively, compared to the control. Cafestol’s effects were dependent on daf-12 (a functional homolog of the human FXR) with upregulation of ech-1.1 (a homolog of enoyl-CoA hydratase involved in fatty acid β-oxidation) and tub-1 (an ortholog of the human TUBBY involved in the neurological regulation of energy expenditure) without any effects on lipogenesis, lipolysis or lipid uptake and transport. Therefore, cafestol increased fat oxidation and energy expenditure via DAF-12-dependent pathway in C. elegans.

The benefits and physiological changes of high intensity interval training

Physical inactivity have been linked with many major non-communicable diseases and as many as 27.5% of adults globally are considered inactive. Physical activity has been proven to be beneficial in the prevention of many chronic diseases and may reduce the risk of premature death. High intensity interval training (HIIT) has been gaining popularity as a time-efficient alternative for regular exercise training. Current studies show that HIIT is more efficient in improving cardiorespiratory fitness, increasing insulin sensitivity and reducing blood pressure than moderate intensity continuous training (MICT). The advantage of HIIT in fat loss compared to MICT is still unclear, but HIIT might be more efficient in the obese population. The effect of HIIT on increasing aerobic fitness could be caused by increase in stroke volume due to the increase in cardiac contractility, capillary density and mitochondrial adaptation. Fat loss during HIIT could be caused by increased fat oxidation and elevated hormones that drive lipolysis and reduce appetite. While vigorous physical activity may transiently increase the risk of cardiac events. The effect of HIIT on increasing aerobic fitness could be caused by increase in stroke volume due to the increase in cardiac contractility, increased of capillary density and mitochondrial adaptation. While fat loss during HIIT could be caused by an increased fat oxidation, elevated hormones that drives lipolysis and reduces appetite. While vigorous physical activity may transiently increase the risk of cardiac event. High intensity interval training is generally safe even in the elderly population and in people with coronary heart disease.

Diurnal influences of fasted and non-fasted brisk walking on gastric emptying rate, metabolic responses, and appetite in healthy males

Growing evidence suggests circadian rhythms, nutrition and metabolism are intimately linked. Intermittent fasting (IMF) has become an increasingly popular intervention for metabolic health and combining IMF with exercise may lead to benefits for weight management. However, little is known about the diurnal variation of fasted exercise. This study aimed to investigate the diurnal influences on gastric emptying rate (GER), metabolic responses, and appetite to fasted and non-fasted exercise. Twelve healthy males completed four 45 min walks in a randomised order. Walks were completed in the morning (AM) and evening (PM) and either fasted (FASTED) or after consumption of a standardised meal (FED). GER of a semi-solid lunch was subsequently measured for 2 h using the 13C breath test. Blood glucose concentration, substrate utilisation, and ratings of appetite were measured throughout. Energy intake was also assessed for the following 24 h. GER Tlag was slower in PM-FASTED compared to AM-FASTED, AM-FED, and PM-FED (75 ± 18 min vs. 63 ± 14 min, P = 0.001, vs. 65 ± 10 min, P = 0.028 and vs. 67 ± 16 min, P = 0.007). Blood glucose concentration was greater in the FED trials in comparison to the FASTED trials pre-lunch (P < 0.05). Fat oxidation was greater throughout exercise in both FASTED trials compared to FED, and remained higher in FASTED trials than fed trials post-exercise until 30 min post-lunch ingestion (all P < 0.05). No differences were found for appetite post-lunch (P > 0.05) or 24 h post-energy intake (P = 0.476). These findings suggest that evening fasted exercise results in delayed GER, without changes in appetite. No compensatory effects were observed for appetite, and 24 h post-energy intake for both fasted exercise trials, therefore, increased fat oxidation holds positive implications for weight management.

Analysis of Direct Effects of the CB1 Receptor Antagonist Rimonabant on Fatty Acid Oxidation and Glycogenolysis in Liver and Muscle Cells in vitro.

Recent pharmacological findings regarding rimonabant, an anorectic and cannabinoid type 1 receptor (CB1R) antagonist, strongly suggest that some of its effects on the metabolic parameters and energy balance in rats are not related to the centrally mediated reduction in caloric intake. Instead, they may be associated with acute induction of glycogenolysis in the liver, in combination with transient increase in glucose oxidation and persistent increase in fat oxidation. It is possible that rimonabant produced direct short- or long-term stimulatory effect on these processes in primary and cultured rat cells. Rimonabant slightly stimulated β-oxidation of long-chain fatty acids in cultured rat myocytes overexpressing glucose transporter isoform 4, as well as activated phosphorylation of adenosine monophosphate-dependent protein kinase (AMPK) in primary rat hepatocytes upon long-term incubation. However, short-term action of rimonabant failed to stimulate β-oxidation in myocytes, myotubes, and hepatocytes, as well as to upregulate AMPK phosphorylation, glycogenolysis, and cAMP levels in hepatocytes. As a consequence, the acute effects of rimonabant on hepatic glycogen content (reduction) and total energy expenditure (increase) in rats fed with a standard diet cannot be explained by direct stimulation of glycogenolysis and fatty acid oxidation in muscles and liver. Rather, these effects seem to be centrally mediated.

Early Time-Restricted Feeding Reduces Appetite and Increases Fat Oxidation But Does Not Affect Energy Expenditure in Humans.

ObjectiveEating earlier in the daytime to align with circadian rhythms in metabolism enhances weight loss. However, it is unknown whether these benefits are mediated through increased energy expenditure or decreased food intake. We therefore performed the first randomized trial to determine how meal timing affects 24-hour energy metabolism when food intake and meal frequency are matched.MethodsEleven overweight adults practiced both early time-restricted feeding (eTRF; eating from 8 am-2 pm) and a control schedule (eating from 8 am-8 pm) each for four days. On the fourth day, 24-hour energy expenditure and substrate oxidation were measured by whole-room calorimetry, in conjunction with appetite and metabolic hormones.ResultseTRF did not affect 24-hour energy expenditure (Δ=10±16 kcal/day; p=0.55). Despite the longer daily fast (intermittent fasting), eTRF decreased mean ghrelin levels by 32±10 pg/ml (p=0.006), made hunger more even-keeled (p=0.006), and tended to increase fullness (p=0.06-0.10) and decrease the desire to eat (p=0.08). eTRF also increased metabolic flexibility (p=0.0006) and decreased the 24-hour non-protein respiratory quotient (Δ=−0.021±0.010; p=0.05).ConclusionsMeal timing interventions facilitate weight loss primarily by decreasing appetite rather than by increasing energy expenditure. eTRF may also increase fat loss by increasing fat oxidation.

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Black Rice Potential in HDL and LDL Profile in Sprague Dawley Rat with High Cholesterol Diet

Atherosclerosis is a significouldt health problem in developed countries and is a major cause of morbidity and mortality, especially in developing countries. Metabolic disorders which include increased levels of LDL and lipoprotein and decreased levels of HDL could cause atherosclerosis which is an inflammatory process due to the formation of plaques on the large artery walls. Black rice is a source of dietary fiber and anthocyanin could act as an antioxidant, which if consumed regularly could improve lipid profiles and blood antioxidants. This is expected to reduce the rate of disease caused by atherosclerosis. The purpose of this study to determine the potential of black rice on HDL and LDL levels in Sprague dawley mice with a high cholesterol diet. This study was in vivo experimental in Sprague dawley rats with a randomized post-test only control group design using 4 groups of rats weighing 175-200g. The group consisted of negative controls, positive controls, simvastatin and black rice drugs. The results showed that rats with hypercholesterol diet which were intervened with black rice feed for 12 weeks decreased LDL and increased HDL. Statistical tests showed that there was a significouldt effect between the treatment of feed on HDL and LDL levels. Further tests showed differences in each group. Conclusion of this study is black rice consumption could regulate lipid profiles by lowering LDL, increasing HDL levels and inhibiting the increase in fat oxidation results in the body with the MDA indicator.

Cafestol Increases Fat Oxidation and Energy Expenditure in Caenorhabditis Elegans via DAF-12-dependent Pathway (OR34-02-19)

ObjectivesCafestol, a diterpene found in coffee beans, is reported to be an agonist of farnesoid X receptors (FXR), nuclear hormone receptors involved in cholesterol homeostasis. It is also known that FXR plays critical roles in other metabolic pathways, including lipid metabolism; however, little is known about cafestol’s effects on lipid metabolism. The goal of the current study was to investigate the effects of cafestol on lipid metabolism using Caenorhabditis elegans as a model system. MethodsC. elegans was treated for 2 days with cafestol or 0.2% dimethyl sulfoxide (vehicle control). Triglycerides, locomotor behavior (an indicator of energy expenditure) and lipid metabolism-related gene expressions were measured. ResultsCafestol at 60 μM significantly reduced fat accumulation by 20% compared to the control. Cafestol increased locomotor activity by 38% compared to the control. The effects of cafestol on fat accumulation were dependent on daf-12 (a functional homolog of the human FXR) and further confirmed by the upregulation of a DAF-12-target gene, fard-1 (the homolog of the human fatty acid reductase 1). Cafestol’s fat-lowering effects were also dependent on tub-1 (an ortholog of the human TUBBY), which is involved in the neurological regulation of energy expenditure. Cafestol upregulated the expression of ech-1.1, involved in fatty acid β-oxidation; however, no effects of cafestol were observed on lipogenesis, lipolysis or lipid uptake and transport. ConclusionsIn conclusion, cafestol regulates lipid metabolism in C. elegans by increasing fatty acid β-oxidation and energy expenditure dependent on daf-12/FXR. Funding SourcesBrazilian National Counsel of Technological and Scientific Development (CNPq).

Phenolic-enriched raspberry fruit extract (Rubus idaeus) resulted in lower weight gain, increased ambulatory activity, and elevated hepatic lipoprotein lipase and heme oxygenase-1 expression in male mice fed a high-fat diet

Red raspberries (Rubus idaeus) contain numerous phenolic compounds with purported health benefits. Raspberry ketone (4-(4-hydroxyphenyl)-2-butanone) is a primary raspberry flavor phenolic found in raspberries and is designated as a synthetic flavoring agent by the Food and Drug Administration. Synthetic raspberry ketone has been demonstrated to result in weight loss in rodents. We tested whether phenolic-enriched raspberry extracts, compared with raspberry ketone, would be more resilient to the metabolic alterations caused by an obesogenic diet. Male C57BL/6J mice (8 weeks old) received a daily oral dose of vehicle (VEH; 50% propylene glycol, 40% water, and 10% dimethyl sulfoxide), raspberry extract low (REL; 0.2 g/kg), raspberry extract high (REH; 2 g/kg), or raspberry ketone (RK; 0.2 g/kg). Coincident with daily dosing, mice were placed on a high-fat diet (45% fat). After 4 weeks, REH and RK reduced body weight gain (approximately 5%-9%) and white adipose mass (approximately 20%) compared with VEH. Hepatic gene expression of heme oxygenase-1 and lipoprotein lipase was upregulated in REH compared with VEH. Indirect calorimetry indicated that respiratory exchange ratio (CO2 production to O2 consumption) was lower, suggesting increased fat oxidation with all treatments. REH treatment increased total ambulatory behavior. Energy expenditure/lean mass was higher in REH compared with REL treatment. There were no treatment differences in cumulative intake, meal patterns, or hypothalamic feed-related gene expression. Our results suggest that raspberry ketone and a phenolic-enriched raspberry extract both have the capacity to prevent weight gain but differ in the preventative mechanisms for excess fat accumulation following high-fat diet exposure.

Exercising with low muscle glycogen content increases fat oxidation and decreases endogenous, but not exogenous carbohydrate oxidation

BackgroundInitiating aerobic exercise with low muscle glycogen content promotes greater fat and less endogenous carbohydrate oxidation during exercise. However, the extent exogenous carbohydrate oxidation increases when exercise is initiated with low muscle glycogen is unclear. PurposeDetermine the effects of muscle glycogen content at the onset of exercise on whole-body and muscle substrate metabolism. MethodsUsing a randomized, crossover design, 12 men (mean ± SD, age: 21 ± 4 y; body mass: 83 ± 11 kg; VO2peak: 44 ± 3 mL/kg/min) completed 2 cycle ergometry glycogen depletion trials separated by 7-d, followed by a 24-h refeeding to elicit low (LOW; 1.5 g/kg carbohydrate, 3.0 g/kg fat) or adequate (AD; 6.0 g/kg carbohydrate, 1.0 g/kg fat) glycogen stores. Participants then performed 80 min of steady-state cycle ergometry (64 ± 3% VO2peak) while consuming a carbohydrate drink (95 g glucose +51 g fructose; 1.8 g/min). Substrate oxidation (g/min) was determined by indirect calorimetry and 13C. Muscle glycogen (mmol/kg dry weight), pyruvate dehydrogenase (PDH) activity, and gene expression were assessed in muscle. ResultsInitiating steady-state exercise with LOW (217 ± 103) or AD (396 ± 70; P < 0.05) muscle glycogen did not alter exogenous carbohydrate oxidation (LOW: 0.84 ± 0.14, AD: 0.87 ± 0.16; P > 0.05) during exercise. Endogenous carbohydrate oxidation was lower and fat oxidation was higher in LOW (0.75 ± 0.29 and 0.55 ± 0.10) than AD (1.17 ± 0.29 and 0.38 ± 0.13; all P < 0.05). Before and after exercise PDH activity was lower (P < 0.05) and transcriptional regulation of fat metabolism (FAT, FABP, CPT1a, HADHA) was higher (P < 0.05) in LOW than AD. ConclusionInitiating exercise with low muscle glycogen does not impair exogenous carbohydrate oxidative capacity, rather, to compensate for lower endogenous carbohydrate oxidation acute adaptations lead to increased whole-body and skeletal muscle fat oxidation.

Combining intermittent fasting with high intensity interval training reduces fat mass by increasing fat oxidation and mobilization

Combining intermittent fasting with high intensity interval training reduces fat mass by increasing fat oxidation and mobilization

Metabolic Consequences of Exposure to Maternal High Fat Diet in Offspring

The increased risk for obesity in offspring born to obese mothers may be driven by changes in energy expenditure. To examine the effects of maternal high fat diet (HFD)‐induced obesity on offspring energy expenditure, female C57BL6/J mice were fed a control (17% fat, TD95092) or HFD (45% fat, TD8811) ad libitum for 12 weeks prior to and during pregnancy and during lactation. Female mice were bred with lean male mice at 17 wk of age. At weaning, male offspring from control and HFD‐dams were randomized to control (C) or HFD (H), provided ad libitum, generating 4 groups of offspring: CC, CH, HC, and HH, where the first letter corresponds to maternal diet and the second to offspring post‐weaning diet. At 20 weeks of age, energy intake and expenditure (EE) were assessed in male offspring over 48 h using the Promethion Continuous Indirect Calorimetry system (Sable Systems). HFD consumption in offspring was associated with reduced respiratory exchange ratio (RER, CC vs CH: 0.89±0.02 vs 0.82±0.02; p&lt;0.01, n=13–16). There was no effect of maternal HFD on offspring RER (CC vs HC, p= 0.66; CH vs HH, p=0.54). To examine the effect of maternal HFD on offspring energy expenditure, ANCOVA using offspring total body weight (measured at the beginning of the indirect calorimety experiment) as a covariate for the 48 h recording period (both light and dark cycles) was performed. When comparing the effect of maternal HFD in offspring fed either a control diet (CC vs HC) or HFD (HC vs HH) postweaning, the covariate (offspring total body weight) significantly predicted EE for both comparisons (CC vs HC, p&lt;0.05; HC vs HH, p = 0.05), while there was no significant effect of maternal diet on EE. Offspring food intake (in both light and dark cycles) was not altered by maternal HFD (CC vs HC, p=0.22; CH vs HH, p=0.21). In control‐fed offspring, maternal HFD had no effect on body weight at 20 wk of age (CC vs CH, 26.84±0.79g vs 28.91±1.03g, p=0.12), while in HFD‐fed offspring, males exposed to maternal HFD were significantly heavier than males from control‐fed dams (CH vs HH, 33.81±1.46g vs 38.42±1.59g, p=0.04). The observed changes in RER indicate that offspring post‐weaning HFD, but not maternal HFD, is associated with a shift in substrate utilization, specifically with increased fat oxidation in response to post‐weaning HFD. In the context of maternal HFD, the EE data suggest that offspring total body weight, and not maternal obesity may be driving offspring changes in energy expenditure.Support or Funding InformationUSDA ARIS Project 6026‐51000‐010‐05SThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Physicochemical and sensory properties of beef muscles after Pulsed Electric Field processing.

This study investigated the effects of pulsed electric field (PEF) processing on the sensory and physicochemical properties of beef biceps femoris (BF) and semitendinosus (ST) muscles. The fresh and frozen-thawed muscles were treated at an electric field strength of 0.8-1.1 kV/cm, pulse width of 20 μs, frequency of 50 Hz and specific energy of 130 kJ/kg. PEF treated samples improved meat tenderness and colour. However increased fat oxidation and increased saturated fatty acids were evident in PEF processed frozen samples. Temporal dominance of sensations results showed that although oxidation was the most dominant in temporal perception, the samples were only found to be detrimental to the sensory quality of PEF processed beef muscles stored for 7 days.

Trans-Cinnamic Acid Stimulates White Fat Browning and Activates Brown Adipocytes.

Recently, pharmacological activation of brown fat and induction of white fat browning (beiging) have been considered promising strategies to treat obesity. To search for natural products that could stimulate the process of browning in adipocytes, we evaluated the activity of trans-cinnamic acid (tCA), a class of cinnamon from the bark of Cinnamomum cassia, by determining genetic expression using real time reverse transcription polymerase chain reaction (RT-PCR) and protein expression by immunoblot analysis for thermogenic and fat metabolizing markers. In our study tCA induced brown like-phenotype in 3T3-L1 white adipocytes and activated HIB1B brown adipocytes. tCA increased protein content of brown-fat-specific markers (UCP1, PRDM16, and PGC-1α) and expression levels of beige-fat-specific genes (Cd137, Cidea, Cited1, Tbx1, and Tmen26) in 3T3-L1 white adipocytes, as well as brown-fat-specific genes (Lhx8, Ppargc1, Prdm16, Ucp1, and Zic1) in HIB1B brown adipocytes. Furthermore, tCA reduced expression of key adipogenic transcription factors C/EBPα and PPARγ in white adipocytes, but enhanced their expressions in brown adipocytes. In addition, tCA upregulates lipid catabolism. Moreover, mechanistic study revealed that tCA induced browning in white adipocytes by activating the β3-AR and AMPK signaling pathways. tCA can induce browning, increase fat oxidation, reduce adipogenesis and lipogenesis in 3T3-L1 adipocytes, and activate HIB1B adipocytes, suggesting its potential to treat obesity.

Impaired fat oxidation during exercise in multiple acyl-CoA dehydrogenase deficiency.

We investigated the in vivo skeletal muscle metabolism in patients with multiple acyl‐CoA dehydrogenase deficiency (MADD) during exercise, and the effect of a glucose infusion. Two adults with MADD on riboflavin and l‐carnitine treatment and 10 healthy controls performed an incremental exercise test measuring maximal oxidative capacity (VO2max) and a submaximal exercise test (≤1 hour) on a cycle ergometer. During submaximal exercise, we studied fat and carbohydrate oxidation, using stable isotope tracer methodology and indirect calorimetry. On another day, the patients repeated the submaximal exercise receiving a 10% glucose infusion. The patients had a lower VO2max than controls and stopped the submaximal exercise test at 51 and 58 minutes due to muscle pain and exhaustion. The exercise‐induced increase in total fatty acid oxidation was blunted in the patients (7.1 and 1.1 vs 12 ± 4 μmol × kg−1 × min−1 in the healthy controls), but total carbohydrate oxidation was higher (67 and 63 vs 25 ± 11 μmol × kg−1 × min−1 in controls). With glucose infusion, muscle pain decreased and average heart rate during exercise dropped in both patients from 124 to 119 bpm and 138 to 119 bpm. We demonstrate that exercise intolerance in MADD‐patients relates to an inability to increase fat oxidation appropriately during exercise, which is compensated partially by an increase in carbohydrate metabolism.

Effect of Wakame and Carob Pod Snacks on Non-Alcoholic Fatty Liver Disease.

Snacks combining different functional ingredients could represent a useful therapeutic strategy against NAFLD. The present study aimed to analyze the effect of two snack formulations based on carob and wakame flour in the treatment for NAFLD in rats. For this purpose, metabolic syndrome was induced in 50 adult rats by a high-fat high-fructose diet over eight weeks. After this period, rats were fed either normal calorie diets supplemented or not with snack A (1/50 wakame/carob pod) and snack B (1/5 wakame/carob pod) for four additional weeks. After sacrifice, liver composition and serum parameters were analyzed. Different pathways of triacylglycerol metabolism in liver were studied including fatty acid oxidation, fatty acid synthesis, triglyceride assembly and release, fatty acid uptake and glucose uptake. Oxidative stress was also measured. Snack treatment, and mainly B snack, reduced liver triacylglycerol levels by increasing fat oxidation. Moreover, this snack reduced oxidative stress. Therefore, this snack formulation could represent an interesting tool useful for fatty liver treatment.

HOW TO EFFECTIVELY BOOST FAT OXIDATION BY CALORIE RESTRICTION IN OVERWEIGHT AND OBESE ADULTS?

Background. It is clinically important to determine the factors that increase fat oxidation and have potential to improve body composition in overweight and obese individuals. Thus, the aim of the present study was to compare the effects of a 2-day very low-calorie diet and 2-day zero-calorie diet on fat oxidation and prospective food consumption in overweight and mildly obese adults. Methods. Eighteen subjects (body mass index above 25 kg/m2) aged 19–33 years were tested under two conditions allocated randomly: 2-day zero-calorie diet with water provided ad libitum and 2-day very-low calorie diet. Appetite sensations, mood state, inhibitory control, and substrate oxidation were evaluated before and after each diet. Results. Greater increase in fat oxidation (p &lt; .05) was observed after zero-calorie diet when compared to a very low-calorie diet. Results showed that both diets increased (p &lt; .05) sensation of hunger and prospective food consumption, whereas no changes were observed in inhibitory control. Greater decrement for vigor (p &lt; .05) was observed after zero-calorie diet when compared to a very low-calorie diet, whereas other mood states were not affected by it. Conclusion. Intermittent fasting with zero-calorie diet may boost fat oxidation to a greater extent when compared to very low-calorie diet and may assist with weight loss in overweight and mildly obese adults.