Muscle Glycogen Synthesis Research Articles

Exogenous Lactate Treatment Immediately after Exercise Promotes Glycogen Recovery in Type-II Muscle in Mice.

Recent studies suggest that lactate intake has a positive effect on glycogen recovery after exercise. However, it is important to verify the effect of lactate supplementation alone and the timing of glycogen recovery. Therefore, in this study, we aimed to examine the effect of lactate supplementation immediately after exercise on glycogen recovery in mice liver and skeletal muscle at 1, 3, and 5 h after exercise. Mice were randomly divided into the sedentary, exercise-only, lactate, and saline-treated groups. mRNA expression and activation of glycogen synthesis and lactate transport-related factors in the liver and skeletal muscle were assessed using real-time polymerase chain reaction. Skeletal muscle glycogen concentration showed an increasing trend in the lactate group compared with that in the control group at 3 and 5 h after post-supplementation. Additionally, exogenous lactate supplementation significantly increased the expression of core glycogen synthesis enzymes, lactate transporters, and pyruvate dehydrogenase E1 alpha 1 in the skeletal muscles. Conversely, glycogen synthesis, lactate transport, and glycogen oxidation to acetyl-CoA were not significantly affected in the liver by exogenous lactate supplementation. Overall, these results suggest that post-exercise lactate supplement enables glycogen synthesis and recovery in skeletal muscles.

New Glycotoxin Inhibitor from Sesuvium sesuvioides Mitigates Symptoms of Insulin Resistance and Diabetes by Suppressing AGE-RAGE Axis in Skeletal Muscle.

The current study intended to investigate the role of new natural compounds derived from the Sesuvium sesuvioides plant in mitigating symptoms of diabetes and insulin resistance in the diabetic mice model. Anti-advanced glycation activity, insulin, and adiponectin were quantified by enzyme-linked immunosorbent assay (ELISA). Glucose uptake was performed using enzymatic fluorescence assay, and glycogen synthesis was measured using PAS staining. Gene and protein expression was assessed using real time PCR (RT-PCR), and immunoblotting and fluorescent microscopy, respectively. The new flavonoid glycoside eupalitin 3-O-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranoside 1 isolated from S. sesuvioides exhibited anti-AGE activity by reducing human glycated albumin in liver cells. In a diabetic mouse model treated with compound 1, we observed improved glucose tolerance, increased adiponectin levels, and decreased insulin resistance. We also observed alleviated AGEs induced reduction in glucose uptake and restored glycogen synthesis in the compound 1-treated diabetic mice muscles. Exploring the molecular mechanism of action in skeletal muscle tissue of diabetic mice, we found that 1 reduced AGE-induced reactive oxygen species and the inflammatory gene in the muscle of diabetic mice. Additionally, 1 exhibited these effects by reducing the gene and protein expression of receptor for advanced glycation end products (RAGE) and inhibiting protein kinase C (PKC) delta activation. This further led us to demonstrate that compound 1 reduced serine phosphorylation of IRS-1, thereby restoring insulin sensitivity. We conclude that a new flavonoid glycoside from S. sesuvioides could be a therapeutic target for the treatment of symptoms of insulin resistance and diabetes.

Small-molecule inhibition of glycogen synthase 1 for the treatment of Pompe disease and other glycogen storage disorders.

Glycogen synthase 1 (GYS1), the rate-limiting enzyme in muscle glycogen synthesis, plays a central role in energy homeostasis and has been proposed as a therapeutic target in multiple glycogen storage diseases. Despite decades of investigation, there are no known potent, selective small-molecule inhibitors of this enzyme. Here, we report the preclinical characterization of MZ-101, a small molecule that potently inhibits GYS1 in vitro and in vivo without inhibiting GYS2, a related isoform essential for synthesizing liver glycogen. Chronic treatment with MZ-101 depleted muscle glycogen and was well tolerated in mice. Pompe disease, a glycogen storage disease caused by mutations in acid α glucosidase (GAA), results in pathological accumulation of glycogen and consequent autophagolysosomal abnormalities, metabolic dysregulation, and muscle atrophy. Enzyme replacement therapy (ERT) with recombinant GAA is the only approved treatment for Pompe disease, but it requires frequent infusions, and efficacy is limited by suboptimal skeletal muscle distribution. In a mouse model of Pompe disease, chronic oral administration of MZ-101 alone reduced glycogen buildup in skeletal muscle with comparable efficacy to ERT. In addition, treatment with MZ-101 in combination with ERT had an additive effect and could normalize muscle glycogen concentrations. Biochemical, metabolomic, and transcriptomic analyses of muscle tissue demonstrated that lowering of glycogen concentrations with MZ-101, alone or in combination with ERT, corrected the cellular pathology in this mouse model. These data suggest that substrate reduction therapy with GYS1 inhibition may be a promising therapeutic approach for Pompe disease and other glycogen storage diseases.

Effects of Subarachnoid Block vs General Anaesthesia on Intraoperative Blood Glucose Levels in Non Diabetic Patients undergoing Elective Surgeries: A Prospective Interventional Study

Introduction: The inhibition of the pituitary gland, an increase in the production of catabolic hormones, and the stimulation of the sympathetic nervous system culminate in surgical stress. These factors result in elevated hepatic glycogenesis and gluconeogenesis, decreased skeletal muscle glucose uptake and glycogen synthesis, and hyperglycaemia. Aim: To examine the effects of Subarachnoid Block (SAB) and General Anaesthesia (GA) on perioperative Capillary Blood Glucose (CBG) levels in individuals undergoing surgery lasting 1-3 hours. Materials and Methods: This prospective interventional study included 100 non diabetic patients undergoing surgery of 1-3 hours duration with 50 patients in each group (GA and SAB). CBG was checked 30 minutes before the administration of anaesthesia, 30 and 60 minutes after the induction of anaesthesia, and 30 minutes after shifting to the Post Anaesthesia Care Unit (PACU) in both the GA and SAB groups. Differences in participant characteristics, such as age and CBG levels in the two groups (SAB and GA), were examined using the two-tailed Independent samples t-test and the Chi-square/ Fisher’s exact test. Results: The mean CBG levels measured 30 minutes before anaesthesia in the GA group were 105.50±21.13 mg/dL, while in the SAB group they were 99.67±19.04 mg/dL, with a p-value of 0.330. However, CBG levels measured 30 minutes after anaesthesia in the GA group were 125.69±22.95 mg/dL, compared to 104.67±20.94 mg/dL in the SAB group, with a p-value of 0.001. At 60 minutes after anaesthesia, CBG levels in the GA group were 152.41±28.97 mg/dL, while in the SAB group they were 99.65±22.69 mg/dL, with a p-value of 0.003. Finally, 30 minutes after shifting to PACU, CBG levels in the GA group were 147.49±27.20 mg/dL, compared to 92.86±24.35 mg/dL in the SAB group, with a p-value of 0.002. Conclusion: CBG levels significantly increased in individuals receiving GA for surgery. This indicates that the hormonal stress response is greater during GA compared to SAB.

Effects of long-term metformin administration associated with high-intensity interval training on physical performance, glycogen concentration, GLUT-4 content, and NMR-based metabolomics in healthy rats.

The aim was to investigate the long-term effects of metformin ingestion on high-intensity interval training on performance, glycogen concentration (GC), GLUT-4 content, and metabolomics outcomes in rats. Fifty male Wistar rats were randomly divided into baseline, metformin (500 mg daily), and control groups. Training consisted of 4 sets of 10 jumps with 30 s of passive recovery per day, 5 days/week for 8 weeks. The intensity equivalent was 50% of body mass (BM) in the first four weeks and 70% of BM in the last four weeks. The animals were submitted to a weekly jump test until exhaustion at 50% of BM. Serum and tissues were collected at baseline and after 4 and 8 weeks for biochemical and metabolomics analysis. The number of jumps increased in the Control group without a significant difference between groups at 4 and 8 weeks. GLUT4 was lower in the gastrocnemius muscle in the Metformin at the fourth week compared to Control (P=0.03) and compared to Metformin (P=0.02) and Control (P=0.01) at eight weeks. Hepatic and soleus GC were not altered by metformin. Gastrocnemius GC was lower after 8 weeks in the Metformin group compared to Control (P=0.01). Significantly lower levels of pyruvate and phenylalanine and higher levels of ethanol, formate, betaine, very low-density lipoprotein, low-density lipoprotein, and creatine were found in the Metformin compared to the Control. Although chronic administration of metformin decreased food intake and negatively influenced the synthesis of muscle glycogen, it did not significantly change physical performance compared to the Control.

Metabolic changes in the subtropical frog Boana pulchella during experimental cooling and recovery conditions

Frogs have developed biochemical and physiological adaptations to occupy diverse ecological niches on Earth successfully. Survival in frozen states is a fascinating strategy made possible by evolving adaptations to produce cryoprotectant solutes. The hylid frog Boana pulchella thrives in South American regions with cold climates, remaining active while enduring sporadic subzero temperatures during winter. The species' metabolic changes during subzero exposure remain unclear. Therefore, we exposed B. pulchella to cooling and recovery, assessing plasma and tissue metabolite changes. Cooling significantly reduced urea concentrations in plasma (P = 0.033), muscle (P = 0.001), heart (P = 0.009), and brain (P = 0.041) compared to acclimation. Liver glucose oxidation and glycogen synthesis were lower in cooling and recovery than in acclimation (P < 0.0001 and P = 0.0117, respectively). Muscle glycogen synthesis was lower in recovery than acclimation (P = 0.0249). These results demonstrate B. pulchella's physiological strategies during subzero exposure, likely reflecting species-specific evolutionary adaptations for brief subzero exposures that enable winter survival in its natural habitat.

Meta-analytic comparison of the effects of consuming carbohydrate with and without protein on postexercise plasma insulin and glucagon responses in healthy, trained males

This meta-analysis evaluates how hydrolysed protein and carbohydrate (CHO) mixtures compare with intact protein and CHO mixtures regarding post-exercise plasma insulin and glucagon responses in healthy endurance trained males. Studies measuring insulin and/or glucagon following an exercise bout with ingestion of CHO vs. CHO+ protein were included. Random-effects meta-analyses were conducted on the insulin peaks over time. Overall, 33 trials from 20 articles were included. The ingestion of CHO+ protein induced significantly higher insulin peaks than ingestion of CHO only from 30 to 240 minutes postexercise (30-180 min: p &lt; .001, 210-240 min: p &lt; .01), higher insulin area under the curve (p &lt; .001), and greater muscle FSR ( p &lt; .001). No statistically significant differences on insulin peaks over time were found between the ingestion of CHO+ intact protein and CHO+ hydrolysed protein or differences in muscle glycogen synthesis rate or glycogen peaks. Findings provide evidence the co-ingestion of CHO+ protein is a better strategy for recovery for endurance-type male athletes than the ingestion of CHO only. However, more research is warranted to understand whether there are differences between the ingestion of intact protein and its hydrolysed counterpart with CHO, and the impact on glucagon responses.

Lysosomal glycogen accumulation in Pompe disease results in disturbed cytoplasmic glycogen metabolism.

Pompe disease is an inherited metabolic myopathy caused by deficiency of acid alpha-glucosidase (GAA), resulting in lysosomal glycogen accumulation. Residual GAA enzyme activity affects disease onset and severity, although other factors, including dysregulation of cytoplasmic glycogen metabolism, are suspected to modulate the disease course. In this study, performed in mice and patient biopsies, we found elevated protein levels of enzymes involved in glucose uptake and cytoplasmic glycogen synthesis in skeletal muscle from mice with Pompe disease, including glycogenin (GYG1), glycogen synthase (GYS1), glucose transporter 4 (GLUT4), glycogen branching enzyme 1 (GBE1), and UDP-glucose pyrophosphorylase (UGP2). Expression levels were elevated before the loss of muscle mass and function. For first time, quantitative mass spectrometry in skeletal muscle biopsies from five adult patients with Pompe disease showed increased expression of GBE1 protein relative to healthy controls at the group level. Paired analysis of individual patients who responded well to treatment with enzyme replacement therapy (ERT) showed reduction of GYS1, GYG1, and GBE1 in all patients after start of ERT compared tobaseline. These results indicate that metabolic changes precede muscle wasting in Pompe disease, and imply a positive feedforward loop in Pompe disease, in which lysosomal glycogen accumulation promotes cytoplasmic glycogen synthesis and glucose uptake, resulting in aggravation of the disease phenotype.

AMPK activation is sufficient to increase skeletal muscle glucose uptake and glycogen synthesis but is not required for contraction-mediated increases in glucose metabolism

The AMP-activated protein kinase (AMPK) is a cellular sensor of energetics and when activated in skeletal muscle during contraction can impart changes in skeletal muscle metabolism. Therapeutics that selectively activate AMPK have been developed to lower glucose levels through increased glucose disposal rates as an approach to abrogate the hyperglycemic state of diabetes; however, the metabolic fate of glucose following AMPK activation remains unclear. We have used a combination of in vivo evaluation of glucose homeostasis and ex vivo skeletal muscle incubation to systematically evaluate metabolism following pharmacological activation of AMPK with PF-739, comparing this with AMPK activation through sustained intermittent electrical stimulation of contraction. These methods to activate AMPK result in increased glucose uptake but divergent metabolism of glucose: pharmacological activation results in increased glycogen accumulation while contraction-induced glucose uptake results in increased lactate formation and glucose oxidation. These results provide additional evidence to support a role for AMPK in control of skeletal muscle metabolism and additional insight into the potential for AMPK stimulation with small molecule direct activators.

Effects of a Very High-Carbohydrate Diet and Endurance Exercise Training on Pancreatic Amylase Activity and Intestinal Glucose Transporter Content in Rats.

We previously reported that the combination of a very high-carbohydrate diet and endurance training increased glucose transporter 4 and glycogen concentration in skeletal muscle. However, it remains unclear whether they also affect the digestive and absorptive capacity in the pancreas and small intestine, which are suggested to be rate-limiting steps in the delivery of exogenous carbohydrates to skeletal muscle and muscle glycogen synthesis. Thus, we aimed to evaluate the effects of a very high-carbohydrate diet and endurance training on pancreatic amylase activity and intestinal glucose transporters in rats and to examine the relationship between these adaptations and their influence on muscle glycogen concentration. Male Sprague-Dawley rats (n=29) were fed a high-carbohydrate diet (59% carbohydrate) or a very high-carbohydrate diet (76% carbohydrate) for 4 wk. Half of the rats in each dietary group were subjected to 6-h swimming exercise training (two 3-h sessions separated by 45 min of rest) for 4 wk. Although there was no significant effect of diet or endurance training on sodium-dependent glucose transporter 1 and glucose transporter 2 contents in the intestine, the rats fed a very high-carbohydrate diet in combination with endurance training had substantially higher pancreatic amylase activity and muscle glycogen concentration. Furthermore, there was a positive correlation between pancreatic amylase activity and muscle glycogen concentration (r=0.599, p=0.001). In conclusion, intake of a very high-carbohydrate diet and endurance training synergistically elevated carbohydrate digestive capacity, which partially accounted for the higher muscle glycogen accumulation.

The effect of coffee consumption on glucose homeostasis and redox-inflammatory responses in high-fat diet-induced obese rats

Coffee effects on glucose homeostasis in obesity remain controversial. We investigated whether coffee mitigates the negative effects on glucose metabolism induced by a high-fat diet and the interrelationships with redox-inflammatory responses. Rats were treated with: control (CT-); coffee (CT+) 3.9 g of freeze-dried coffee/kg of diet; high-fat (HF-); or high-fat + coffee 3.9 g of freeze-dried coffee/kg of diet (HF+) diet. The high-fat diet increased weight gain, feed efficiency, HOMA β, muscle and hepatic glycogen, intestinal CAT and SOD activity, hepatic protein (CARB) and lipid oxidation (MDA), muscle Prkaa1 mRNA and IL6 levels, and decreased food intake, hepatic GR, GPX and SOD activities, intestinal CARB, intestinal Slc2a2 and Slc5a1 and hepatic Prkaa1 and Prkaa2 mRNA levels, hepatic glucose-6-phosphatase and muscle hexokinase (HK) activities, compared to the control diet. The high-fat diet with coffee increased hepatic GST activity and TNF and decreased IL6 and intestinal glucosidase activity compared with the high-fat diet. The coffee diet increased muscle glycogen, hepatic CARB and PEPCK activity, and decreased hepatic GR and SOD activities and intestinal CARB, compared with the control diet. Coffee increased insulin levels, HOMA IR/β, FRAP, muscle Prkaa1 mRNA levels and hepatic and muscle phosphofructokinase-1, and it decreased intestinal CAT, hepatic Slc2a2 mRNA levels and muscle HK activity, regardless of the diet type. In conclusion, chronic coffee consumption improves antioxidant and anti-inflammatory responses, but does not ameliorate glucose homeostasis in a high-fat diet-induced obesity model. In addition, coffee consumption increases insulin secretion and promotes muscle glycogen synthesis in rats maintained on a control diet.

Alkaloidal extract from Zanthoxylum zanthoxyloides stimulates insulin secretion in normoglycemic and nicotinamide/streptozotocin-induced diabetic rats

IntroductionIncrease in the prevalence of type-2 diabetes in Sub-Sahara Africa has created the need for robust treatment and management programs. However, an effective diabetes management program requires a high annual budget that most countries in this region cannot afford. That said, various plants and plant products in this region have either been confirmed and/or ethnopharmacologically used for the management of type-2 diabetes. AimTo investigate the antidiabetic and insulin secretory effects of an alkaloidal extract derived from Zanthoxylum zanthoxyloides in normoglycemic and experimental diabetic rats. Materials and methodsAlkaloidal extract was prepared from leaves of Zanthoxylum zanthoxyloides (ZZAE). Nicotinamide/streptozotocin-induced type-2 diabetes was modeled in male Sprague Dawley rats weighing between 130 to 150 g. The experimental diabetic rats were grouped into six treatment groups [Model, 20% Tween20, chlorpropamide, and ZZAE (50, 100, and 150 mg/kg)], and one control group. Fasting blood glucose (FBG), and body weight were measured weekly. Rats were sacrificed 2 days after treatment under chloroform anesthesia to collect blood samples and to isolate major organs for biochemical, and histological analyses respectively. Islets of Langerhans were isolated from normoglycemic rats and co-cultured with ZZAE and chlorpropamide (10 μg/mL) to assess the insulin secretory effect of ZZAE. ResultsZZAE improved glucose kinetics curve in normoglycemic (p < 0.001) and experimental diabetic rats (p < 0.05) compared to the model. ZZAE (100 and 150 mg/kg) restored islets population, and improved kidney, and liver, histoarchitecture. ZZAE (150 mg/kg) improved post-treatment serum insulin levels compared to the model group (p < 0.001) and the Chlorpropamide group (p < 0.05). ZZAE also restored glycogen synthesis in skeletal muscles of experimental diabetic rats and stimulated insulin secretion in pancreatic islets of Langerhans isolated from normoglycemic rats. ConclusionThese results showed that ZZAE has active alkaloids that can be explored for diabetes management.

High Carbohydrate Diet Increased Glucose Transporter Protein Levels in Jejunum but Did Not Lead to Enhanced Post-Exercise Skeletal Muscle Glycogen Recovery.

We examined the effect of dietary carbohydrate intake on post-exercise glycogen recovery. Male Institute of Cancer Research (ICR) mice were fed moderate-carbohydrate chow (MCHO, 50%cal from carbohydrate) or high-carbohydrate chow (HCHO, 70%cal from carbohydrate) for 10 days. They then ran on a treadmill at 25 m/min for 60 min and administered an oral glucose solution (1.5 mg/g body weight). Compared to the MCHO group, the HCHO group showed significantly higher sodium-D-glucose co-transporter 1 protein levels in the brush border membrane fraction (p = 0.003) and the glucose transporter 2 level in the mucosa of jejunum (p = 0.004). At 30 min after the post-exercise glucose administration, the skeletal muscle and liver glycogen levels were not significantly different between the two diet groups. The blood glucose concentration from the portal vein (which is the entry site of nutrients from the gastrointestinal tract) was not significantly different between the groups at 15 min after the post-exercise glucose administration. There was no difference in the total or phosphorylated states of proteins related to glucose uptake and glycogen synthesis in skeletal muscle. Although the high-carbohydrate diet significantly increased glucose transporters in the jejunum, this adaptation stimulated neither glycogen recovery nor glucose absorption after the ingestion of post-exercise glucose.

DHA/EPA Improves GLUT4 Translocation, Glycogen Synthesis and Aerobic Glycolysis in Skeletal Muscle of db/db Mice

Abstract Objectives The aim of this study was to investigate the effects of DHA and EPA on glucose metabolism including glucose uptake and disposal in skeletal muscle and C2C12 myotubes. Methods Four-week-old db/db diabetic mice were fed with control diet enriched with DHA/EPA (purity &amp;gt; 99%, 1% wt/wt) for 10 weeks. To further explore the underlying mechanism, C2C12 myotubes were induced insulin resistance by palmitate and treated with 25 and 50 μM DHA/EPA for 24 h after differentiation. Results The untargeted metabolome of skeletal muscle showed BCAAs and other metabolites associated with glycolysis and TCA cycle were altered by DHA/EPA treatment. Further detections revealed DHA/EPA treatment promoted the translocation of GLUT4 via increasing Rab8a and SNAP23 expression, and enhanced the activity of GS and PDH. In vitro, the glucose consumption was improved coupled with promoted Rab8a or SNAP23, and GS and PDH were also activated under DHA/EPA intervention increased glucose consumption via promoted Rab8a and SNAP23. The GS and PDH were also activated, which were in line with the results in vivo. Conclusions Long-term intake of DHA and EPA may have a protective effect on diabetes through promoted GLUT4 translocation, glycogen synthesis and aerobic glycolysis in skeletal muscle. Funding Sources This work was supported by the National Natural Science Foundation of China (grant number 81773419 and 81300309), Chinese Institute of Nutrition DSM Research Fund (grant number CNS-DSM-2017–035), China National Program for Support of Top-notch Young Professionals and China Postdoctoral Science Foundation (grant number 2020M681869).

Photobiomodulation therapy ameliorates hyperglycemia and insulin resistance by activating cytochrome c oxidase-mediated protein kinase B in muscle.

Ameliorating hyperglycemia and insulin resistance are major therapeutic strategies for type 2 diabetes. Previous studies have indicated that photobiomodulation therapy (PBMT) attenuates metabolic abnormalities in insulin-resistant adipose cells and tissues. However, it remains unclear whether PBMT ameliorates glucose metabolism in skeletal muscle in type 2 diabetes models. Here we showed that PBMT reduced blood glucose and insulin resistance, and reversed metabolic abnormalities in skeletal muscle in two diabetic mouse models. PBMT accelerated adenosine triphosphate (ATP) and reactive oxygen species (ROS) generation by elevating cytochrome c oxidase (CcO) activity. ROS-induced activation of phosphatase and tensin homolog (PTEN)/ protein kinase B (AKT) signaling after PBMT promoted glucose transporter GLUT4 translocation and glycogen synthase (GS) activation, accelerating glucose uptake and glycogen synthesis in skeletal muscle. CcO subunit III deficiency, ROS elimination, and AKT inhibition suppressed the PBMT effects of glucose metabolism in skeletal muscle. This study indicated amelioration of glucose metabolism after PBMT in diabetic mouse models and revealed the metabolic regulatory effects and mechanisms of PBMT on skeletal muscle.

Perspective: Ketone Supplementation in Sports—Does It Work?

Oral ketone supplements have gained popularity in recent years. There is biological rationale for a potential ergogenic effect of this type of supplement, as they might not only alter muscle fuel preference during exercise (and promote glycogen sparing, with potential benefits for endurance performance) but also favor cognition performance during exertion or muscle glycogen synthesis after exercise. However, as discussed in this Perspective, evidence to date does not support a benefit of acute ketone supplementation on sports performance, cognition, or muscle recovery [although further research with long-duration exercise (i.e., >60min), is needed], and the evidence for chronic supplementation is sparse. In addition, acute intake of ketone supplements might be associated with gastrointestinal symptoms, and further research is warranted on the long-term safety of repeated use of ketone supplements. In summary, there is currently insufficient evidence to support the overall effectiveness of ketone supplements in sports.

Dietary Supplementation with Exogenous Sea-Cucumber-Derived Ceramides and Glucosylceramides Alleviates Insulin Resistance in High-Fructose-Diet-Fed Rats by Upregulating the IRS/PI3K/Akt Signaling Pathway.

Endogenous ceramide is considered to be associated with the progress of insulin resistance. However, the effects of dietary exogenous glucosylceramides and ceramides on insulin resistance are unclear. A model of fructose-induced male Sprague Dawley rats was used to compare the effects of sea-cucumber-derived glucosylceramides and ceramides on insulin resistance. Both glucosylceramides and ceramides significantly improved glucose tolerance, reduced the concentrations of serum glucose and glycosylated hemoglobin, and alleviated the accompanied hypertension. Ceramides significantly enhanced glycogen levels in skeletal muscle, whereas glucosylceramides significantly increased the hepatic glycogen levels. Moreover, glucosylceramides alleviated insulin resistance by inhibiting gluconeogenesis, promoting glycogen synthesis and insulin signal transduction in the liver; meanwhile, ceramides were mainly due to the promotion of glycogen synthesis and insulin signal transduction in skeletal muscle. Additionally, glucosylceramides and ceramides effectively attenuated inflammation in adipose tissue. These results indicate that glucosylceramides and ceramides have potential value in the prevention and alleviation of insulin resistance.

Skeletal muscle glycogen synthesis - it turns out we still know very little.

Skeletal muscle glycogen synthesis - it turns out we still know very little.

Effects of posthatch feed deprivation on residual yolk absorption, macronutrients synthesis, and organ development in broiler chicks

The aim of the research was to evaluate the dynamic changes of early posthatch starvation on residual yolk absorption, synthesis of macronutrients (protein, lipid, and glycogen), and organ development in broiler chicks. A total of 720 1-day-old chicks (Lingnan Yellow) were randomly assigned to 3 treatments: group A (nonfasted), group B (fasting for 24 h after placement), and group C (fasting for 48 h after placement). The trial lasted for 168 h, and water was provided ad libitum all the time. Sampling was performed at 0, 24, 48, 72, 120, and 168 h. Nonfasting (group A) promoted (P < 0.05) the absorption of amino acids, fatty acids, mineral elements, protein, and maternal antibody in the residual yolk of broiler chicks. The concentration of insulin-like growth factor 1 in plasma and the liver was higher (P < 0.05) in group A. Nonfasting enhanced (P < 0.05) the synthesis of protein and glycogen in the breast muscle and liver; the relative weights of the liver, pancreas, and spleen; and body weight, but retarded (P < 0.05) the synthesis of triglyceride in the liver. The results indicated that nonfasting (group A) after placement promoted the absorption of residual yolk and synthesis of protein and glycogen in the breast muscle and liver, whereas early feed deprivation promoted the synthesis of lipid in the liver. Thereby, nonfasting after placement promoted organ development and body growth of broiler chicks.

Coingestion of Carbohydrate and Protein on Muscle Glycogen Synthesis after Exercise: A Meta-analysis.

Evidence suggests that carbohydrate and protein (CHO-PRO) ingestion after exercise enhances muscle glycogen repletion to a greater extent than carbohydrate (CHO) alone. However, there is no consensus at this point, and results across studies are mixed, which may be attributable to differences in energy content and carbohydrate intake relative to body mass consumed after exercise. The purpose of this study was determine the overall effects of CHO-PRO and the independent effects of energy and relative carbohydrate content of CHO-PRO supplementation on postexercise muscle glycogen synthesis compared with CHO alone. Meta-analysis was conducted on crossover studies assessing the influence of CHO-PRO compared with CHO alone on postexercise muscle glycogen synthesis. Studies were identified in a systematic review from PubMed and Cochrane Library databases. Data are presented as effect size (95% confidence interval [CI]) using Hedges' g. Subgroup analyses were conducted to evaluate effects of isocaloric and nonisocaloric energy content and dichotomized by median relative carbohydrate (high, ≥0.8 g·kg-1⋅h-1; low, <0.8 g·kg-1⋅h-1) content on glycogen synthesis. Twenty studies were included in the analysis. CHO-PRO had no overall effect on glycogen synthesis (0.13, 95% CI = -0.04 to 0.29) compared with CHO. Subgroup analysis found that CHO-PRO had a positive effect (0.26, 95% CI = 0.04-0.49) on glycogen synthesis when the combined intervention provided more energy than CHO. Glycogen synthesis was not significant (-0.05, 95% CI = -0.23 to 0.13) in CHO-PRO compared with CON when matched for energy content. There was no statistical difference of CHO-PRO on glycogen synthesis in high (0.07, 95% CI = -0.11 to 0.22) or low (0.21, 95% CI = -0.08 to 0.50) carbohydrate content compared with CHO. Glycogen synthesis rates are enhanced when CHO-PRO are coingested after exercise compared with CHO only when the added energy of protein is consumed in addition to, not in place of, carbohydrate.