Browsing by Author "Starck CS"
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- ItemCytotoxic aggregation and amyloid formation by the myostatin precursor protein(Public Library of Science, 2010) Starck CS; Sutherland Smith AJMyostatin, a negative regulator of muscle growth, has been implicated in sporadic inclusion body myositis (sIBM). sIBM is the most common age-related muscle-wastage disease with a pathogenesis similar to that of amyloid disorders such as Alzheimer's and Parkinson's diseases. Myostatin precursor protein (MstnPP) has been shown to associate with large molecular weight filamentous inclusions containing the Alzheimer's amyloid beta peptide in sIBM tissue, and MstnPP is upregulated following ER stress. The mechanism for how MstnPP contributes to disease pathogenesis is unknown. Here, we show for the first time that MstnPP is capable of forming amyloid fibrils in vitro. When MstnPP-containing Escherichia coli inclusion bodies are refolded and purified, a proportion of MstnPP spontaneously misfolds into amyloid-like aggregates as characterised by electron microscopy and binding of the amyloid-specific dye thioflavin T. When subjected to a slightly acidic pH and elevated temperature, the aggregates form straight and unbranched amyloid fibrils 15 nm in diameter and also exhibit higher order amyloid structures. Circular dichroism spectroscopy reveals that the amyloid fibrils are dominated by β-sheet and that their formation occurs via a conformational change that occurs at a physiologically relevant temperature. Importantly, MstnPP aggregates and protofibrils have a negative effect on the viability of myoblasts. These novel results show that the myostatin precursor protein is capable of forming amyloid structures in vitro with implications for a role in sIBM pathogenesis.
- ItemDietary thiols in exercise: oxidative stress defence, exercise performance, and adaptation(BioMed Central, 2017) McLeay Y; Stannard S; Houltham S; Starck CSEndurance athletes are susceptible to cellular damage initiated by excessive levels of aerobic exercise-produced reactive oxygen species (ROS). Whilst ROS can contribute to the onset of fatigue, there is increasing evidence that they play a crucial role in exercise adaptations. The use of antioxidant supplements such as vitamin C and E in athletes is common; however, their ability to enhance performance and facilitate recovery is controversial, with many studies suggesting a blunting of training adaptations with supplementation. The up-regulation of endogenous antioxidant systems brought about by exercise training allows for greater tolerance to subsequent ROS, thus, athletes may benefit from increasing these systems through dietary thiol donors. Recent work has shown supplementation with a cysteine donor (N-acetylcysteine; NAC) improves antioxidant capacity by augmenting glutathione levels and reducing markers of oxidative stress, as well as ergogenic potential through association with delayed fatigue in numerous experimental models. However, the use of this, and other thiol donors may have adverse physiological effects. A recent discovery for the use of a thiol donor food source, keratin, to potentially enhance endogenous antioxidants may have important implications for endurance athletes hoping to enhance performance and recovery without blunting training adaptations.
- ItemNutrient Dense, Low-Cost Foods Can Improve the Affordability and Quality of the New Zealand Diet-A Substitution Modeling Study(MDPI (Basel, Switzerland), 2021-07-27) Starck CS; Blumfield M; Keighley T; Marshall S; Petocz P; Inan-Eroglu E; Abbott K; Cassettari T; Ali A; Wham C; Kruger R; Kira G; Fayet-Moore FThe high prevalence of non-communicable disease in New Zealand (NZ) is driven in part by unhealthy diet selections, with food costs contributing to an increased risk for vulnerable population groups. This study aimed to: (i) identify the nutrient density-to-cost ratio of NZ foods; (ii) model the impact of substituting foods with a lower nutrient density-to-cost ratio with those with a higher nutrient density-to-cost ratio on diet quality and affordability in representative NZ population samples for low and medium socioeconomic status (SES) households by ethnicity; and (iii) evaluate food processing level. Foods were categorized, coded for processing level and discretionary status, analyzed for nutrient density and cost, and ranked by nutrient density-to-cost ratio. The top quartile of nutrient dense, low-cost foods were 56% unprocessed (vegetables, fruit, porridge, pasta, rice, nuts/seeds), 31% ultra-processed (vegetable dishes, fortified bread, breakfast cereals unfortified <15 g sugars/100 g and fortified 15–30 g sugars/100 g), 6% processed (fruit juice), and 6% culinary processed (oils). Using substitution modeling, diet quality improved by 59% and 71% for adults and children, respectively, and affordability increased by 20–24%, depending on ethnicity and SES. The NZ diet can be made healthier and more affordable when nutritious, low-cost foods are selected. Processing levels in the healthier, modeled diet suggest that some non-discretionary ultra-processed foods may provide a valuable source of low-cost nutrition for food insecure populations.
- ItemToward a Dynamic Model of Indispensable Amino Acid Requirements of the Adult Human: A Factorial Estimate of Oxidative Amino Acid Losses.(Elsevier B.V., 2024-11-02) Starck CS; Wolfe RR; Moughan PJBackground Consensus regarding the required intake of indispensable amino acids (IDAAs) and protein [representing total amino acids (AAs)] in the adult is lacking. Oxidation is a major, although not exclusive, source of IDAA loss in humans body and a primary factor determining requirements; a quantitative understanding of oxidative IDAA losses is required. Objectives This study aimed to develop a factorial diurnal model of total oxidative IDAA and protein losses in the adult human. Methods A factorial diurnal model of oxidative losses of protein and each IDAA at maintenance was developed by estimating the magnitude and variability of sources of oxidative loss from existing literature: inevitable catabolism (constitutive oxidation of each absorbed dietary AA), and protein turnover in the postprandial and postabsorptive states. Total oxidative losses were calculated by summing individual losses, validated against published independent nitrogen balance data and compared with current IDAA requirements. Results The factorial model predicted minimum oxidative total AA losses of 390 ± 60 mg/kg BW/d, 59% of the estimated average requirement for protein. Inevitable AA oxidation and oxidation associated with postabsorptive protein turnover were the major sources of the oxidative loss for protein, at 40% and 44%, respectively. Summed oxidative IDAA losses ranged from 64% (isoleucine) to 91% (tryptophan) of current requirements. Total oxidative losses predicted by the model were significant predictors of actual experimental oxidative losses obtained by nitrogen balance (R2 = 0.66; P = 0.049). Conclusions The use of a factorial model for estimation of minimum IDAA and protein oxidative losses in the adult human provides an essential starting point for an updated understanding of protein and IDAA requirements. Further iterations of the model will estimate total protein and IDAA requirements, and account for variations in dietary protein quantity and quality, as well as different populations and physiologic states. Additional data, especially for inevitable oxidation in humans, and particularly with respect to individual IDAAs, are needed.