Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

Jiménez-Maldonado, Alberto; Virgen-Ortíz, Adolfo; Melnikov, Valery; Rodríguez-Hernández, Alejandrina; Gamboa‐Domínguez, Armando; Montero, Sergio; Muñiz-Murguía, Jesús; Lemus, Mónica; Álvarez-Buylla, Elena Roces de

doi:10.1080/19382014.2016.1260796

Cited by 12 publications

(10 citation statements)

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“…It is well established that acute exercise increases circulating BDNF [ 35 ] and may represent a “dose” of BDNF [ 31 ], analogous to rodent infusion studies. For instance, 8 weeks of treadmill training increases plasma BDNF in healthy rats and BDNF appears to mediate the exercise-induced improvements in insulin tolerance and increased beta cell size [ 14 , 27 ]. Accordingly, exercise may improve diabetes risk factors and obesity directly through its effects on glucose regulation and energy expenditure, as well as indirectly via its effects on BDNF and improvements in glucose regulation and metabolic health from exercise.…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, increasing BDNF levels improves metabolic regulation, as intracerebroventricular infusion of exogenous BDNF suppresses appetite [ 24 , 25 ] and improves systemic glycemic control via hepatocyte insulin sensitivity [ 26 ], pancreatic beta cell function [ 14 , 27 ], and increased glucose utilization [ 28 ] in animal models. Further, overexpression of hypothalamic BDNF in mice facilitates the browning of adipose tissue via sympathetic nerve activity, leading to increased energy expenditure and reduced plasma glucose levels [ 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

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Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

et al. 2018

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Obesity in youth increases the risk of type 2 diabetes (T2D), and both are risk factors for neurocognitive deficits. Exercise attenuates the risk of obesity and T2D while improving cognitive function. In adults, these benefits are associated with the actions of the brain-derived neurotrophic factor (BDNF), a protein critical in modulating neuroplasticity, glucose regulation, fat oxidation, and appetite regulation in adults. However, little research exists in youth. This study examined the associations between changes in diabetes risk factors and changes in BDNF levels after 6 months of exercise training in adolescents with obesity. The sample consisted of 202 postpubertal adolescents with obesity (70% females) aged 14–18 years who were randomized to 6 months of aerobic and/or resistance training or nonexercise control. All participants received a healthy eating plan designed to induce a 250/kcal deficit per day. Resting serum BDNF levels and diabetes risk factors, such as fasting glucose, insulin, homeostasis model assessment (HOMA-B—beta cell insulin secretory capacity) and (HOMA-IS—insulin sensitivity), and hemoglobin A1c (HbA1c), were measured after an overnight fast at baseline and 6 months. There were no significant intergroup differences on changes in BDNF or diabetes risk factors. In the exercise group, increases in BDNF were associated with reductions in fasting glucose (β = −6.57, SE = 3.37, p = 0.05) and increases in HOMA-B (β = 0.093, SE = 0.03, p = 0.004) after controlling for confounders. No associations were found between changes in diabetes risk factors and BDNF in controls. In conclusion, exercise-induced reductions in some diabetes risk factors were associated with increases in BDNF in adolescents with obesity, suggesting that exercise training may be an effective strategy to promote metabolic health and increases in BDNF, a protein favoring neuroplasticity. This trial is registered with ClinicalTrials.gov NCT00195858, September 12, 2005 (funded by the Canadian Institutes of Health Research).

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

et al. 2018

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“…Moreover, uncoupling proteins (UCPs) play a pivotal role in the metabolic adaptation of BAT to exercise training, increasing the oxidation of metabolic substrates necessary for sustaining enhanced thermogenesis in order to produce heat ( Boss et al, 1998 ; Ricquier, 2006 ). On the other hand, it has been described that chronic exercise improves insulin sensitivity ( Wagner et al, 2016 ; Jimenez-Maldonado et al, 2017 ), favoring glucose uptake in the muscle ( Kim, 2016 ), controlling glucose tolerance ( Molsted et al, 2013 ), as well as preventing vascular dysfunction ( Lee et al, 2011 ). However, there is nothing described whether exercise might improve insulin sensitivity in BAT and what mechanisms might be involved in such improvement.…”

Section: Introductionmentioning

confidence: 99%

Chronic Exercise Improves Mitochondrial Function and Insulin Sensitivity in Brown Adipose Tissue

et al. 2018

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The aim of the present work was to study the consequences of chronic exercise training on factors involved in the regulation of mitochondrial remodeling and biogenesis, as well as the ability to produce energy and improve insulin sensitivity and glucose uptake in rat brown adipose tissue (BAT). Male Wistar rats were divided into two groups: (1) control group (C; n = 10) and (2) exercise-trained rats (ET; n = 10) for 8 weeks on a motor treadmill (five times per week for 50 min). Exercise training reduced body weight, plasma insulin, and oxidized LDL concentrations. Protein expression of ATP-independent metalloprotease (OMA1), short optic atrophy 1 (S-OPA1), and dynamin-related protein 1 (DRP1) in BAT increased in trained rats, and long optic atrophy 1 (L-OPA1) and mitofusin 1 (MFN1) expression decreased. BAT expression of nuclear respiratory factor type 1 (NRF1) and mitochondrial transcription factor A (TFAM), the main factors involved in mitochondrial biogenesis, was higher in trained rats compared to controls. Exercise training increased protein expression of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) and AMP-activated protein kinase (pAMPK/AMPK ratio) in BAT. In addition, training increased carnitine palmitoyltransferase II (CPT II), mitochondrial F1 ATP synthase α-chain, mitochondrial malate dehydrogenase 2 (mMDH) and uncoupling protein (UCP) 1,2,3 expression in BAT. Moreover, exercise increased insulin receptor (IR) ratio (IRA/IRB ratio), IRA-insulin-like growth factor 1 receptor (IGF-1R) hybrids and p42/44 activation, and decreased IGF-1R expression and IR substrate 1 (p-IRS-1) (S307) indicating higher insulin sensitivity and favoring glucose uptake in BAT in response to chronic exercise training. In summary, the present study indicates that chronic exercise is able to improve the energetic profile of BAT in terms of increased mitochondrial function and insulin sensitivity.

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“…Exercise can improve insulin sensitivity and thereby alter skeletal muscle glucose transport and maintain blood glucose homeostasis, especially for patients with metabolic disease [ 36 ], but may not always have the same effect in athletes due to excessive production of ROS during exercise training [ 37 , 38 , 39 ]. In this study, we did not detect a significant reduction in glucose parameters in the ubiquinone group after supplementation; however, we found that athletes with higher WBC ubiquinone level (≥0.5 nmol/g) showed improved glycemic control ( Table 3 and Figure 2 ), which might be related to an increase in antioxidant capacity ( Table 4 ).…”

Section: Discussionmentioning

confidence: 99%

Ubiquinone Supplementation with 300 mg on Glycemic Control and Antioxidant Status in Athletes: A Randomized, Double-Blinded, Placebo-Controlled Trial

Chang

Chen

et al. 2020

Antioxidants

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The aim of this study is to investigate the glycemic profile, oxidative stress, and antioxidant capacity in athletes after 12 weeks of ubiquinone supplementation. It was a double-blinded, randomized, parallel, placebo-controlled study. Thirty-one well-trained college athletes were randomly assigned to ubiquinone (300 mg/d, n = 17) or placebo group (n = 14). The glycemic profile [fasting glucose, glycated hemoglobin (HbA1c), homeostatic model assessment-insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI)], plasma and erythrocyte malondialdehyde (MDA), total antioxidant capacity (TAC), and ubiquinone status were measured. After supplementation, the plasma ubiquinone concentration was significantly increased (p < 0.05) and the level of erythrocyte MDA was significantly lower in the ubiquinone group than in the placebo group (p < 0.01). There was a significant correlation between white blood cell (WBC) ubiquinone and glycemic parameters [HbA1c, r = −0.46, p < 0.05; HOMA-IR, r = −0.67, p < 0.01; QUICKI, r = 0.67, p < 0.01]. In addition, athletes with higher WBC ubiquinone level (≥0.5 nmol/g) showed higher erythrocyte TAC and QUICKI and lower HOMA-IR. In conclusion, we demonstrated that athletes may show a better antioxidant capacity with higher ubiquinone status after 12 weeks of supplementation, which may further improve glycemic control.

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Effect of moderate and high intensity chronic exercise on the pancreatic islet morphometry in healthy rats: BDNF receptor participation

Cited by 12 publications

References 49 publications

Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

Changes in the Brain-Derived Neurotrophic Factor Are Associated with Improvements in Diabetes Risk Factors after Exercise Training in Adolescents with Obesity: The HEARTY Randomized Controlled Trial

Chronic Exercise Improves Mitochondrial Function and Insulin Sensitivity in Brown Adipose Tissue

Ubiquinone Supplementation with 300 mg on Glycemic Control and Antioxidant Status in Athletes: A Randomized, Double-Blinded, Placebo-Controlled Trial

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