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12. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

Author

Reynolds, Joseph C, Lai, Rochelle W, Woodhead, Jonathan ST, Joly, James H, Mitchell, Cameron J, Cameron-Smith, David, Lu, Ryan, Cohen, Pinchas, Graham, Nicholas A, Benayoun, Bérénice A, Merry, Troy L, and Lee, Changhan

Subjects
Biochemistry and Cell Biology, Health Sciences, Sports Science and Exercise, Biological Sciences, Aging, Prevention, Nutrition, Stem Cell Research - Nonembryonic - Non-Human, Genetics, Stem Cell Research, Underpinning research, 1.1 Normal biological development and functioning, Musculoskeletal, Adult, Animals, Cell Line, Cell Nucleus, Gene Expression Regulation, Homeostasis, Humans, Male, Metabolomics, Mice, Mice, Inbred C57BL, Mitochondria, Mitochondria, Muscle, Mitochondrial Proteins, Muscle, Skeletal, Myoblasts, Stress, Physiological, Young Adult
Abstract

Healthy aging can be promoted by enhanced metabolic fitness and physical capacity. Mitochondria are chief metabolic organelles with strong implications in aging that also coordinate broad physiological functions, in part, using peptides that are encoded within their independent genome. However, mitochondrial-encoded factors that actively regulate aging are unknown. Here, we report that mitochondrial-encoded MOTS-c can significantly enhance physical performance in young (2 mo.), middle-age (12 mo.), and old (22 mo.) mice. MOTS-c can regulate (i) nuclear genes, including those related to metabolism and proteostasis, (ii) skeletal muscle metabolism, and (iii) myoblast adaptation to metabolic stress. We provide evidence that late-life (23.5 mo.) initiated intermittent MOTS-c treatment (3x/week) can increase physical capacity and healthspan in mice. In humans, exercise induces endogenous MOTS-c expression in skeletal muscle and in circulation. Our data indicate that aging is regulated by genes encoded in both of our co-evolved mitochondrial and nuclear genomes.

Published
2021

14. Fish oil supplementation during pregnancy and postpartum in mothers with overweight and obesity to improve body composition and metabolic health during infancy: A double-blind randomized controlled trial

Author

Satokar, Vidit V., Derraik, José G.B., Harwood, Matire, Okesene-Gafa, Karaponi, Beck, Kathryn, Cameron-Smith, David, Garg, Manohar L., O’Sullivan, Justin M., Sundborn, Gerhard, Pundir, Shikha, Mason, R Preston, Cutfield, Wayne S., and Albert, Benjamin B.

Published
2023
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18. Digoxin and exercise effects on skeletal muscle Na+,K+‐ATPase isoform gene expression in healthy humans.

Author

McKenna, Michael J., Gong, Xiaofei, Petersen, Aaron C., Sostaric, Simon, Goodman, Craig A., Garnham, Andrew, Aw, Tai‐Juan, Steward, Collene H., Murphy, Kate T., Carey, Kate A., Krum, Henry, Snow, Rodney J., and Cameron‐Smith, David

Subjects
GENE expression, EXERCISE physiology, GENETIC regulation, DIGOXIN, SKELETAL muscle, GINGER
Abstract

In muscle, digoxin inhibits Na+,K+‐ATPase (NKA) whereas acute exercise can increase NKA gene expression, consistent with training‐induced increased NKA content. We investigated whether oral digoxin increased NKA isoform mRNA expression (qPCR) in muscle at rest, during and post‐exercise in 10 healthy adults, who received digoxin (DIG, 0.25 mg per day) or placebo (CON) for 14 days, in a randomised, double‐blind and cross‐over design. Muscle was biopsied at rest, after cycling 20 min (10 min each at 33%, then 67% V̇O2peak${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{peak}}}}$), then to fatigue at 90% V̇O2peak${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{peak}}}}$ and 3 h post‐exercise. No differences were found between DIG and CON for NKA α1–3 or β1–3 isoform mRNA. Both α1 (354%, P = 0.001) and β3 mRNA (P = 0.008) were increased 3 h post‐exercise, with α2 and β1–2 mRNA unchanged, whilst α3 mRNA declined at fatigue (−43%, P = 0.045). In resting muscle, total β mRNA (∑(β1+β2+β3)) increased in DIG (60%, P = 0.025) and also when transcripts for each isoform were normalised to CON then either summed (P = 0.030) or pooled (n = 30, P = 0.034). In contrast, total α mRNA (∑(α1+α2+α3), P = 0.348), normalised then summed (P = 0.332), or pooled transcripts (n = 30, P = 0.717) did not differ with DIG. At rest, NKA α1–2 and β1–2 protein abundances were unchanged by DIG. Post‐exercise, α1 and β1–2 proteins were unchanged, but α2 declined at 3 h (19%, P = 0.020). In conclusion, digoxin did not modify gene expression of individual NKA isoforms at rest or with exercise, indicating NKA gene expression was maintained consistent with protein abundances. However, elevated resting muscle total β mRNA with digoxin suggests a possible underlying β gene‐stimulatory effect. Highlights: What is the central question of this study?Na+,K+‐ATPase (NKA) in muscle is important for Na+/K+ homeostasis. We investigated whether the NKA‐inhibitor digoxin stimulates increased NKA gene expression in muscle and exacerbates NKA gene responses to exercise in healthy adults.What is the main finding and its importance?Digoxin did not modify exercise effects on muscle NKA α1–3 and β1–3 gene transcripts, which comprised increased post‐exercise α1 and β3 mRNA and reduced α3 mRNA during exercise. However, in resting muscle, digoxin increased NKA total β isoform mRNA expression. Despite inhibitory‐digoxin or acute exercise stressors, NKA gene regulation in muscle is consistent with the maintenance of NKA protein contents. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Protein Intake and Physical Activity Levels as Determinants of Sarcopenia Risk in Community-Dwelling Older Adults.

Author

Stoodley, Isobel L., Berthon, Bronwyn S., Scott, Hayley A., Williams, Evan J., Baines, Penelope J., Knox, Hannah, Wood, Sophie, Paradzayi, Beauty, Cameron-Smith, David, and Wood, Lisa G.

Abstract

Community screening for sarcopenia is complex, with barriers including access to specialized equipment and trained staff to conduct body composition, strength and function assessment. In the current study, self-reported dietary protein intake and physical activity (PA) in adults ≥65 years was assessed relative to sarcopenia risk, as determined by body composition, strength and physical function assessments, consistent with the European Working Group on Sarcopenia in Older People (EWGSOP) definition. Of those screened (n = 632), 92 participants (77% female) were assessed as being at high risk of developing sarcopenia on the basis of dietary protein intake ≤1 g∙kg−1∙day−1 [0.9 (0.7–0.9) g∙kg−1∙day−1] and moderate intensity physical activity <150 min.week−1. A further 31 participants (65% female) were defined as being at low risk, with both protein intake [1.2 (1.1–1.5) g∙kg−1∙day−1] and PA greater than the cut-off values. High-risk participants had reduced % lean mass [53.5 (7.8)% versus 54.8 (6.1)%, p < 0.001] and impaired strength and physical function. Notably, high-risk females exhibited greater deficits in lean mass and strength, with minimal differences between groups for males. In community-dwelling older adults, self-reported low protein intake and low weekly PA is associated with heightened risk for sarcopenia, particularly in older women. Future research should determine whether early intervention in older adults with low protein intake and PA attenuates functional decline. [ABSTRACT FROM AUTHOR]

Published
2024
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32. B vitamin and one-carbon metabolite profiles show divergent associations with cardiometabolic risk markers but not cognitive function in older New Zealand adults: A secondary analysis of the REACH Study

Author

Gillies, Nicola A., primary, Milan, Amber M., additional, Cameron-Smith, David, additional, Mumme, Karen D., additional, Conlon, Cathryn A., additional, von Hurst, Pamela R., additional, Haskell-Ramsay, Crystal F., additional, Jones, Beatrix, additional, Roy, Nicole C., additional, Coad, Jane, additional, Wall, Clare R., additional, and Beck, Kathryn L., additional

Published
2023
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35. Cold water immersion in recovery following a single bout resistance exercise suppresses mechanisms of miRNA nuclear export and maturation

Author

D'Souza, Randall F., primary, Figueiredo, Vandre C., additional, Markworth, James F., additional, Zeng, Nina, additional, Hedges, Christopher P., additional, Roberts, Llion A., additional, Raastad, Truls, additional, Coombes, Jeff S., additional, Peake, Jonathan M., additional, Mitchell, Cameron J., additional, and Cameron‐Smith, David, additional

Published
2023
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39. Safety, Tolerability, and Pharmacokinetics of β-Cryptoxanthin Supplementation in Healthy Women: A Double-Blind, Randomized, Placebo-Controlled Clinical Trial

Author

Tan, Karen M. L., primary, Chee, Jolene, additional, Lim, Kezlyn L. M., additional, Ng, Maisie, additional, Gong, Min, additional, Xu, Jia, additional, Tin, Felicia, additional, Natarajan, Padmapriya, additional, Lee, Bee Lan, additional, Ong, Choon Nam, additional, Tint, Mya Thway, additional, Kee, Michelle Z. L., additional, Müller-Riemenschneider, Falk, additional, Gluckman, Peter D., additional, Meaney, Michael J., additional, Kumar, Mukkesh, additional, Karnani, Neerja, additional, Eriksson, Johan G., additional, Nandanan, Bindu, additional, Wyss, Adrian, additional, and Cameron-Smith, David, additional

Published
2023
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43. Fish oil supplementation during pregnancy and postpartum in mothers with overweight and obesity to improve body composition and metabolic health during infancy : A double-blind randomized controlled trial

Author

V. Satokar, Vidit, Derraik, José G. B., Harwood, Matire, Okesene-Gafa, Karaponi, Beck, Kathryn, Cameron-Smith, David, Garg, Manohar L., O'Sullivan, Justin M., Sundborn, Gerhard, Pundir, Shikha, Mason, R. Preston, Cutfield, Wayne S., Albert, Benjamin B., V. Satokar, Vidit, Derraik, José G. B., Harwood, Matire, Okesene-Gafa, Karaponi, Beck, Kathryn, Cameron-Smith, David, Garg, Manohar L., O'Sullivan, Justin M., Sundborn, Gerhard, Pundir, Shikha, Mason, R. Preston, Cutfield, Wayne S., and Albert, Benjamin B.

Abstract

Background: Maternal obesity during pregnancy is associated with an increased risk of obesity and metabolic disease in the offspring. Supplementation with fish oil (FO), which is insulin sensitizing, during pregnancy in mothers with overweight or obesity may prevent the development of greater adiposity and metabolic dysfunction in their children. Objectives: To determine the effects of FO supplementation throughout the second half of pregnancy and lactation in mothers with overweight or obesity on infant body composition and metabolism. Methods: A double-blind randomized controlled trial of 6 g FO (3.55 g/d of n-3 PUFAs) compared with olive oil (control) from mid-pregnancy until 3 mo postpartum. Eligible women had singleton pregnancies at 12-20 wk of gestation, and BMI >= 25 kg/m2. The primary outcome was the infant body fat percentage (DXA scans) at 2 wk of age. Secondary outcomes included maternal metabolic markers during pregnancy, infant anthropometry at 2 wk and 3 mo of age, and metabolic markers at 3 mo. Results: A total of 129 mothers were randomized, and 98 infants had a DXA scan at 2 wk. Primary outcome: Imputed and nonimputed analyses showed no effects of FO supplementation on infant body fat percentage at age 2 wk. Secondary outcomes: There were no treatment effects on infant outcomes at 2 wk, but FO infants had a higher BMI z-score (P = 0.025) and ponderal index (P = 0.017) at age 3 mo. FO supplementation lowered maternal tri-glycerides by 17% at 30 wk of pregnancy (P = 0.0002) and infant triglycerides by 21% at 3 mo of age (P = 0.016) but did not affect maternal or infant insulin resistance. The rate of emergency cesarean section was lower with FO supplementation [aRR = 0.38 (95%CI 0.16, 0.90); P = 0.027]. Conclusions: FO supplementation of mothers with overweight or obesity during pregnancy did not impact infant body composition. There is a need to follow up the offspring to determine whether the observed metabolic effects persist. Clinical trial re

Published
2023
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