Interaction between Lipid Availability, Endurance Exercise and Insulin Sensitivity

2014 ◽  
pp. 62-70 ◽  
Author(s):  
Sean A. Newsom ◽  
Simon Schenk
Keyword(s):  
Insulin Sensitivity ◽  
Endurance Exercise

Corrigendum: An acute bout of endurance exercise but not sprint interval exercise enhances insulin sensitivity

2009 ◽  
Vol 34 (2) ◽  
pp. 306-306
Author(s):  
Jonathan R. Brestoff ◽  
Benjamin Clippinger ◽  
Thomas Spinella ◽  
Serge P. von Duvillard ◽  
Bradley C. Nindl ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Endurance Exercise ◽  
Acute Bout ◽  
Interval Exercise

Adeno-Associated Virus-Mediated Knockdown of SLC16A11 Improves Glucose Tolerance and Hepatic Insulin Signaling in High Fat Diet-Fed Mice

2019 ◽  
Author(s):  
Tan Zhang ◽  
Zhengtang Qi ◽  
Haiyan Wang ◽  
Shuzhe Ding
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Endurance Exercise ◽  
Insulin Signaling ◽  
High Fat Diet ◽  
Exercise Stress ◽  
High Fat ◽  
Adeno Associated Virus ◽  
Hepatic Insulin Signaling ◽  
The Impact

Abstract Background SLC16A11, a member of the SLC16 family, is associated with lipid metabolism, causing increased intracellular triacylglycerol (TAG) levels. In the current study, our primary goal was to determine if an SLC16A11 knockdown would improve glucose tolerance and hepatic insulin signaling in high fat diet (HFD)–fed mice. Additionally, the mechanism for exercise-improved insulin sensitivity remains unclear, and there is no mechanistic insight into SLC16A11’s role in insulin sensitivity under exercise stress. Therefore, we also examined the impact of endurance exercise on the abundance of SLC16A11. Methods C57BL/6 J male mice were fed either regular chow (Control) or HFD for 8 weeks and then injected with adeno-associated virus (AAV). Plasma parameters, tissue lipid contents, glucose tolerance, and expression profiles of hepatic insulin signaling were detected. Also, other mice were divided randomly into sedentary and exercise groups. We assessed hepatic expression of SLC16A11 after 8 weeks of endurance exercise. Results 1) Hepatic SLC16A11 expression was greater in HFD-fed mice compared to Control mice. 2) AAV-mediated knockdown of SLC16A11 improved glucose tolerance, prevented TAG accumulation in serum and liver, and increased phosphorylation of protein kinase B (Akt) and glycogen synthesis kinase-3β (GSK3β) in HFD-fed mice. 3) Endurance exercise decreased hepatic SLC16A11 expression. Conclusions Inactivation of SLC16A11, which is robustly induced by HFD, improved glucose tolerance and hepatic insulin signaling, independent of body weight, but related to TAG. Additionally, SLC16A11 might mediate the health benefits of endurance exercise.

scholarly journals High-fat diet impairs the effects of a single bout of endurance exercise on glucose transport and insulin sensitivity in rat skeletal muscle

Metabolism ◽  
2007 ◽  
Vol 56 (12) ◽  
pp. 1719-1728 ◽  
Author(s):  
Satsuki Tanaka ◽  
Tatsuya Hayashi ◽  
Taro Toyoda ◽  
Taku Hamada ◽  
Yohei Shimizu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Endurance Exercise ◽  
High Fat Diet ◽  
High Fat ◽  
Rat Skeletal Muscle ◽  
Single Bout

scholarly journals Genomics and transcriptomics landscapes associated to changes in insulin sensitivity in response to endurance exercise training

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Louise Y. Takeshita ◽  
Peter K. Davidsen ◽  
John M. Herbert ◽  
Philipp Antczak ◽  
Matthijs K. C. Hesselink ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Molecular Mechanisms ◽  
Calcium Signalling ◽  
Sensitivity Index ◽  
Transcriptional Signature ◽  
Endurance Exercise Training ◽  
Causative Effect ◽  
Exercise Induced

AbstractDespite good adherence to supervised endurance exercise training (EET), some individuals experience no or little improvement in peripheral insulin sensitivity. The genetic and molecular mechanisms underlying this phenomenon are currently not understood. By investigating genome-wide variants associated with baseline and exercise-induced changes (∆) in insulin sensitivity index (Si) in healthy volunteers, we have identified novel candidate genes whose mouse knockouts phenotypes were consistent with a causative effect on Si. An integrative analysis of functional genomic and transcriptomic profiles suggests genetic variants have an aggregate effect on baseline Si and ∆Si, focused around cholinergic signalling, including downstream calcium and chemokine signalling. The identification of calcium regulated MEF2A transcription factor as the most statistically significant candidate driving the transcriptional signature associated to ∆Si further strengthens the relevance of calcium signalling in EET mediated Si response.

An acute bout of endurance exercise but not sprint interval exercise enhances insulin sensitivity

2009 ◽  
Vol 34 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Jonathan R. Brestoff ◽  
Benjamin Clippinger ◽  
Thomas Spinella ◽  
Serge P. von Duvillard ◽  
Bradley Nindl ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Endurance Exercise ◽  
Plasma Concentrations ◽  
Intervention Strategy ◽  
Whole Body ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Acute Bout ◽  
Interval Exercise ◽  
Highly Correlated

An acute bout of endurance exercise (EE) enhances insulin sensitivity, but the effects of sprint interval exercise (SIE) have not yet been described. We sought to compare insulin sensitivity at baseline and after an acute bout of EE and SIE in healthy men (n = 8) and women (n = 5) (age, 20.7 ± 0.3 years; peak oxygen consumption (VO2 peak), 42.6 ± 1.7 mL·kg–1·min–1; <1.5 days·week–1 structured exercise; body fat, 21.1 ± 1.9%). Subjects underwent 3 oral glucose tolerance tests (OGTTs) the day after each of the following 3 conditions: no exercise, baseline (OGTTB); SIE at ~125% VO2 peak (OGTTSIE); and EE at ~75% VO2 peak (OGTTEE). SIE and EE sessions were randomized for each subject. Subjects consumed identical meals the day preceding each OGTT. Two insulin sensitivity indices — composite whole-body insulin sensitivity index (ISI-COMP) and ISI-hepatic insulin sensitivity (HOMA) — were calculated, using previously validated formulas (ISI-COMP = 10 000/√(glucosefasting × insulinfasting × glucosemean OGTT × insulinmean OGTT); ISI-HOMA = 22.5/(insulinfasting × glucosefasting)), and the plasma concentrations of cytokines interleukin-6 and tumor necrosis factor-α were measured. There were no differences by sex for any condition (men vs. women, p > 0.05). Pearson’s correlation coefficients between ISI-COMP and ISI-HOMA for each condition were highly correlated (p < 0.01), and followed similar patterns of response. ISI-COMPEE was 71.4% higher than ISI-COMPB (8.4 ± 1.4 vs. 4.9 ± 1.0; p < 0.01) and 40.0% higher than ISI-COMPSIE (8.4 ± 1.4 vs. 6.0 ± 1.5; p < 0.05), but there was no difference between ISI-COMPB and ISI-COMPSIE (p = 0.182). VO2 peak was highly correlated with both ISI-COMP and ISI-HOMA during baseline and SIE test conditions (p < 0.02). These findings demonstrate that an acute bout of EE, but not SIE, increases insulin sensitivity relative to a no-exercise control condition in healthy males and females. While these findings underscore the use of regular EE as an effective intervention strategy against insulin resistance, additional research examining repeated sessions of SIE on insulin sensitivity is warranted.

Interactive effects of acute exercise and carbohydrate-energy replacement on insulin sensitivity in healthy adults.

2021 ◽  
Author(s):  
Drusus A Johnson-Bonson ◽  
Benjamin J Narang ◽  
Russell G Davies ◽  
Aaron Hengist ◽  
Harry A Smith ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Endurance Exercise ◽  
Acute Exercise ◽  
Treadmill Exercise ◽  
Interactive Effects ◽  
Energy Deficit ◽  
Whole Body ◽  
Oral Glucose ◽  
Postprandial Glycemia ◽  
Energy Replacement

This study investigated whether carbohydrate-energy replacement immediately after prolonged endurance exercise attenuates insulin sensitivity the following morning, and whether exercise improves insulin sensitivity the following morning independent of an exercise-induced carbohydrate deficit. Oral glucose tolerance and whole-body insulin sensitivity were compared the morning after three evening conditions, involving: (1) treadmill exercise followed by carbohydrate replacement drink (200 or 150 g maltodextrin for males and females, respectively; CHO-replace); (2) treadmill exercise followed by a non-caloric, taste-matched placebo (CHO-deficit); or (3) seated rest with no drink provided (Rest). Treadmill exercise involved 90 minutes at ~80% age-predicted maximum heart rate. Seven males and two females (aged 23 ± 1 years; body mass index 24.0 ± 2.7 kg·m-2) completed all conditions in a randomized order. Matsuda index improved by 22% (2.2 [0.3, 4.0] au, p = .03) and HOMA2-IR improved by 10% (-0.04 [-0.08, 0.00] au, p = .04) in CHO-deficit versus CHO-replace, without corresponding changes in postprandial glycemia. Outcomes were similar between Rest and other conditions. These data suggest that improvements to insulin sensitivity in healthy populations following acute moderate/vigorous intensity endurance exercise may be dependent on the presence of a carbohydrate-energy deficit. NOVELTY • Restoration of carbohydrate balance following acute endurance exercise attenuated whole-body insulin sensitivity • Exercise per se failed to enhance whole-body insulin sensitivity • Maximizing or prolonging the post-exercise carbohydrate deficit may enhance acute benefits to insulin sensitivity

scholarly journals Molecular adaptations in human subcutaneous adipose tissue after ten weeks of endurance exercise training in healthy males

2019 ◽  
Vol 126 (3) ◽  
pp. 569-577 ◽  
Author(s):  
Simon Riis ◽  
Britt Christensen ◽  
Birgitte Nellemann ◽  
Andreas Buch Møller ◽  
Anna Sofie Husted ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Subcutaneous Adipose Tissue ◽  
Control Group ◽  
Hexokinase Ii ◽  
Endurance Exercise Training ◽  
Associated Proteins ◽  
Subcutaneous Adipose

Endurance exercise training induces adaptations in metabolically active organs, but adaptations in human subcutaneous adipose tissue (scAT) remains incompletely understood. On the basis of animal studies, we hypothesized that endurance exercise training would increase the expression of proteins involved in lipolysis and glucose uptake in scAT. To test these hypotheses, 19 young and healthy males were randomized to either endurance exercise training (TR; age 18–24 yr; BMI 19.0–25.4 kg/m2) or a nonexercising control group (CON; age 21–35 yr; BMI 20.5–28.8 kg/m2). Abdominal subcutaneous fat biopsies and blood were obtained at rest before and after intervention. By using Western blotting and PCR, we determined expression of lipid droplet-associated proteins, various proteins involved in substrate metabolism, and mRNA abundance of cell surface G protein-coupled receptors (GPCRs). Adipose tissue insulin sensitivity was determined from fasting plasma insulin and nonesterified fatty acids (adipose tissue insulin resistance index; Adipo-IR). Adipo-IR improved in TR compared with CON ( P = 0.03). This was accompanied by increased insulin receptor (IR) protein expression in scAT with a 1.54-fold (SD 0.79) change from baseline in TR vs. 0.85 (SD 0.30) in CON ( P = 0.007). Additionally, hexokinase II (HKII) and succinate dehydrogenase complex subunit A (SDHA) protein increased in TR compared with CON ( P = 0.006 and P = 0.04, respectively). We did not observe changes in lipid droplet-associated proteins or mRNA abundance of GPCRs. Collectively, 10 weeks of endurance exercise training improved adipose tissue insulin sensitivity, which was accompanied by increased IR, HKII, and SDHA protein expression in scAT. We suggest that these adaptations contribute to an improved metabolic flexibility. NEW & NOTEWORTHY This study is the first to investigate the molecular adaptations in human subcutaneous adipose tissue (scAT) after endurance exercise training compared with a nonexercising control group. We show that endurance exercise training improves insulin sensitivity in human scAT, and this is accompanied by increased expression of insulin receptor, hexokinase II, and succinate dehydrogenase complex subunit A. Collectively, our data suggest that endurance exercise training induces molecular adaptations in human scAT, which may contribute to an improved metabolic flexibility.

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