Exercise training protects human and rodent β cells against endoplasmic reticulum stress and apoptosis

Paula, Flávia M.; Leite, Nayara C.; Borck, Patrícia Cristine; Freitas-Dias, Ricardo; Cnop, Miriam; Chacon-Mikahil, Mara Patrícia Traina; Cavaglieri, Cláudia Regina; Marchetti, Piero; Boschero, Antônio Carlos; Zoppi, Cláudio C.; Eizirik, Décio L.

doi:10.1096/fj.201700710r

Cited by 36 publications

(46 citation statements)

References 52 publications

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“…These findings were corroborated by an independent study, using a similar experimental design. Serum taken from healthy humans following endurance training (8 weeks of cycling at ∼70%

{\dot{V}}_{O_{2} \max}

, 1 h per day, 5 days per week) protected EndoC‐βH1 and primary human islets cells against apoptosis induced by pro‐inflammatory cytokines (IL‐1β and IFN‐γ) (Paula et al., 2018).…”

Section: Effect Of Exercise On β‐Cell Masssupporting

confidence: 58%

“…Within these categories, we have tried to clarify the mechanism through which these effects manifest (Table 1). β‐Cell mass can be influenced through effects on β‐cell proliferation (Calegari et al., 2012, Kiraly et al., 2007, Kiraly et al., 2008, Li et al., 2013), apoptosis or increased viability (Calegari et al., 2012, Choi, Jang, Hong, Jun, & Park, 2006, Park, Hong, Lee, Sung, & Kim, 2008, Paula et al., 2015, Paula et al., 2018). β‐Cell function can be influenced through effects on glucose sensing, insulin content and insulin secretion.…”

Section: Introductionmentioning

confidence: 99%

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The benefits of physical exercise for the health of the pancreatic β‐cell: a review of the evidence

Curran

Drayson

Zoppi

et al. 2020

Experimental Physiology

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Physical exercise is a core therapy for type 1 and type 2 diabetes. Whilst the benefits of exercise for different physiological systems are recognised, the effect of exercise specifically on the pancreatic -cell is not well described. Here we review the effects of physical exercise on -cell health.We show that exercise improves -cell mass and function. The improved function manifests primarily through the increased insulin content of the -cell and its increased ability to secrete insulin in response to a glucose stimulus. We review the evidence relating to glucose sensing, insulin signalling, -cell proliferation and -cell apoptosis in humans and animal models with acute exercise and following exercise training programmes. Some of the mechanisms through which these benefits manifest are discussed. K E Y W O R D S

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“…These findings were corroborated by an independent study, using a similar experimental design. Serum taken from healthy humans following endurance training (8 weeks of cycling at ∼70%

{\dot{V}}_{O_{2} \max}

, 1 h per day, 5 days per week) protected EndoC‐βH1 and primary human islets cells against apoptosis induced by pro‐inflammatory cytokines (IL‐1β and IFN‐γ) (Paula et al., 2018).…”

Section: Effect Of Exercise On β‐Cell Masssupporting

confidence: 58%

Section: Introductionmentioning

confidence: 99%

The benefits of physical exercise for the health of the pancreatic β‐cell: a review of the evidence

Curran

Drayson

Zoppi

et al. 2020

Experimental Physiology

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“…Although the mechanisms underlying on cancer prevention and progression are still not fully understood, there is evidence that chronic moderate exercise induce several desirable metabolic alterations, such as reducing fat cell volume ( Nechuta et al, 2015 ; Pistor et al, 2015 ), improving tissue insulin sensitivity and reducing fasting hyperinsulinemia ( Westerlind et al, 2003 ; Gomes et al, 2013 ; Keshel and Coker, 2015 ) and increase pancreatic beta-cell function and mass ( Calegari et al, 2012 ; Gomes et al, 2013 ; Paula et al, 2018 ; Veloso et al, 2018 ). This information is very important, because during tumor growth and cell proliferation, weak pancreatic insulin secretion is present ( Fernandes et al, 1990 ; Rose and Vona-Davis, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

Aerobic Exercise Training Attenuates Tumor Growth and Reduces Insulin Secretion in Walker 256 Tumor-Bearing Rats

et al. 2018

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Aerobic exercise training can improve insulin sensitivity in many tissues; however, the relationship among exercise, insulin, and cancer cell growth is unclear. We tested the hypothesis that aerobic exercise training begun during adolescence can attenuate Walker 256 tumor growth in adult rats and alter insulin secretion. Thirty-day-old male Wistar rats engaged in treadmill running for 8 weeks, 3 days/week, 44 min/day, at 55–65% VO2max until they were 90 days old (TC, Trained Control). An equivalently aged group was kept inactive during the same period (SC, Sedentary Control). Then, half the animals of the SC and TC groups were reserved as the control condition and the other half were inoculated with Walker 256 cancer cells, yielding two additional groups (Sedentary Walker and Trained Walker). Zero mortalities were observed in tumor-bearing rats. Body weight (BW), food intake, plasma glucose, insulin levels, and peripheral insulin sensitivity were analyzed before and after tumor cell inoculation. We also evaluated tumor growth, metastasis and cachexia. Isolated pancreatic islets secretory activity was analyzed. In addition, we evaluated mechanic sensibility. Our results showed improved physical performance according to the final workload and VO2max and reduced BW in trained rats at the end of the running protocol. Chronic adaptation to the aerobic exercise training decreased tumor weight, cachexia and metastasis and were associated with low glucose and insulin levels and high insulin sensitivity before and after tumor cell inoculation. Aerobic exercise started at young age also reduced pancreatic islet insulin content and insulin secretion in response to a glucose stimulus, without impairing islet morphology in trained rats. Walker 256 tumor-bearing sedentary rats also presented reduced pancreatic islet insulin content, without changing insulin secretion through isolated pancreatic islets. The mechanical sensitivity test indicated that aerobic exercise training did not cause injury or trigger inflammatory processes prior to tumor cell inoculation. Taken together, the current study suggests that aerobic exercise training applied during adolescence may mitigate tumor growth and related disorders in Walker 256 tumor-bearing adult rats. Improved insulin sensibility, lower glucose and insulin levels and/or reduced insulin secretion stimulated by glucose may be implicated in this tumor attenuation.

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“…Such regulation could be mediated by myokines, protein factors secreted from SkM . For example, exercise is known to improve/protect β-cell viability (Narendran et al, 2017;Paula et al, 2018) at least in part through IL6 released from SkM, either acting directly on β-cells (Christensen et al, 2015;Paula et al, 2015), or by enhancing GLP-1 secretion from L cells and alpha cells (Ellingsgaard et al, 2011). Yet, others have found no effects of physiologic levels of IL6 on insulin secretion .…”

Section: Discussionmentioning

confidence: 99%

Myokine Regulation of Insulin Secretion: Impact of Inflammation and Type 2 Diabetes

2020

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Skeletal muscle (SkM) secretes protein factors (myokines) that can exert multiple actions. To study the control of myokine regulation of β-cell function, SkM biopsies were taken from non-diabetic (ND) and Type 2 diabetic (T2D) subjects and satellite cells cultured to myotubes (MT). MT were also treated with lipopolysaccharide (infectious inflammation-II) or a combination of glucose (10 mM), insulin (120 pM), and palmitate (0.4 mM) (metabolic inflammation-MI) to model the inflammatory and metabolic conditions seen in vivo with T2D. Conditioned media (CM) was collected from MT after 24 h and used to treat INS-1 cells for 24 h. Cell viability, total insulin content, glucose-stimulated insulin secretion (GSIS) and maximal (IBMX-stimulated) IS (IS max) were monitored. Under baseline conditions, CM from ND and T2D MT had no effects on INS-1 cell viability, insulin content, GSIS, or IS max. After exposure to II, CM from ND-MT augmented GSIS in INS-1 cells by 100 ± 25% over control (p < 0.05); T2D-CM had no effect. After exposure to MI, T2D-CM suppressed GSIS by 35 ± 5% (p < 0.05); ND-CM was without effect. Under either of these conditions cell viability, total insulin content and IS max were unaffected. Effects of CM on GSIS were lost after CM was boiled. Both augmentation of GSIS by ND-CM from II-treated MT, and suppression by T2D-CM from MI-treated MT, were inhibited by wortmannin, Ro 31-8220, and SB203580. In summary: (1) ND-MT are able to augment GSIS when stressed, (2) T2D-MT responding to a diabetic-like environment secrete myokines that suppress GSIS, (3) Unknown protein factors exert effects specifically on GSIS, possibly through PI-3K, PKC, and/or p38 MAPK. In T2D, both insulin resistance and a suppression of adaptive increased insulin secretion are intrinsic properties of SkM that can contribute to the full T2D phenotype.

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Exercise training protects human and rodent β cells against endoplasmic reticulum stress and apoptosis

Cited by 36 publications

References 52 publications

The benefits of physical exercise for the health of the pancreatic β‐cell: a review of the evidence

The benefits of physical exercise for the health of the pancreatic β‐cell: a review of the evidence

Aerobic Exercise Training Attenuates Tumor Growth and Reduces Insulin Secretion in Walker 256 Tumor-Bearing Rats

Myokine Regulation of Insulin Secretion: Impact of Inflammation and Type 2 Diabetes

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