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Aims: To examine the effects of a high‐fat‐diet (HFD) on monogenic neonatal diabetes, without the confounding effects of compensatory hyperinsulinaemia. Methods: Mice expressing KATP channel gain‐of‐function (KATP‐GOF) mutations, which models human neonatal diabetes, were fed an HFD. Results: Surprisingly, KATP‐GOF mice exhibited resistance to HFD‐induced obesity, accompanied by markedly divergent blood glucose control, with some KATP‐GOF mice showing persistent diabetes (KATP‐GOF‐non‐remitter [NR] mice) and others showing remission of diabetes (KATP‐GOF‐remitter [R] mice). Compared with the severely diabetic and insulin‐resistant KATP‐GOF‐NR mice, HFD‐fed KATP‐GOF‐R mice had lower blood glucose, improved insulin sensitivity, and increased circulating plasma insulin and glucagon‐like peptide‐1 concentrations. Strikingly, while HFD‐fed KATP‐GOF‐NR mice showed increased food intake and decreased physical activity, reduced whole body fat mass and increased plasma lipids, KATP‐GOF‐R mice showed similar features to those of control littermates. Importantly, KATP‐GOF‐R mice had restored insulin content and β‐cell mass compared with the marked loss observed in both HFD‐fed KATP‐GOF‐NR and chow‐fed KATP‐GOF mice. Conclusion: Together, our results suggest that restriction of dietary carbohydrates and caloric replacement by fat can induce metabolic changes that are beneficial in reducing glucotoxicity and secondary consequences of diabetes in a mouse model of insulin‐secretory deficiency. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) elicits pleiotropic physiological effects ranging from modulation of cardiovascular to CNS functions. A dominant method for transmission of sulfide-based signals is via posttranslational modification of reactive cysteine thiols to persulfides. However, the source of the persulfide donor and whether its relationship to H2S is as a product or precursor is controversial. The transsulfuration pathway enzymes can synthesize cysteine persulfide (Cys-SSH) from cystine and H2S from cysteine and/or homocysteine. Recently, Cys-SSH was proposed as the primary product of the transsulfuration pathway with H2S representing a decomposition product of Cys-SSH. Our detailed kinetic analyses demonstrate a robust capacity for Cys-SSH production by the human transsulfuration pathway enzymes, cystathionine beta-synthase and γ-cystathionase (CSE) and for homocysteine persulfide synthesis from homocystine by CSE only. However, in the reducing cytoplasmic milieu where the concentration of reduced thiols is significantly higher than of disulfides, substrate level regulation favors the synthesis of H2S over persulfides. Mathematical modeling at physiologically relevant hepatic substrate concentrations predicts that H2S rather than Cys-SSH is the primary product of the transsulfuration enzymes with CSE being the dominant producer. The half-life of the metastable Cys-SSH product is short and decomposition leads to a mixture of polysulfides (Cys-S-(S)n-S-Cys). These in vitro data, together with the intrinsic reactivity of Cys-SSH for cysteinyl versus sulfur transfer, are consistent with the absence of an observable increase in protein persulfidation in cells in response to exogenous cystine and evidence for the formation of polysulfides under these conditions. [ABSTRACT FROM AUTHOR]

The article discusses the study regarding the training methods in baseball pitchers. It examines the impact of peak throwing velocity, and stamina methods in pitchers. It analyzes the essence of a battling ropes training program (BRT), and a running program (RP) on 18 Division II collegiate baseball pitchers who were assigned into two groups. It notes that the BRT has physiological consequences on upper body peak oxygen uptake, and oxygen consumption power output after training.

The article discusses the results of a study that determined the physiological attributes that affect the distance-running performance of collegiate distance runners. It examines the relationship among running economy (RE), maximal aerobic capacity, anaerobic threshold (AT) and ventilatory threshold (VT). The relationship of performance pace velocity and RE was not strong across the common economy velocities. It concludes that AT pace is the strongest predictor of distance-running performance.

The coming years are likely to be turbulent due to a myriad of factors or polycrisis, including an escalation in climate extremes, emerging public health threats, weak productivity, increases in global economic instability and further weakening in the integrity of global democracy. These formidable challenges are not exogenous to the economy but are in some cases generated by the system itself. They can be overcome, but only with far-reaching changes to global economics. Our current socio-economic paradigm is insufficient for addressing these complex challenges, let alone sustaining human development, well-being and happiness. To support the flourishing of the global population in the age of polycrisis, we need a novel, person-centred and collective paradigm. The brain economy leverages insights from neuroscience to provide a novel way of centralising the human contribution to the economy, how the economy in turn shapes our lives and positive feedbacks between the two. The brain economy is primarily based on Brain Capital, an economic asset integrating brain health and brain skills, the social, emotional, and the diversity of cognitive brain resources of individuals and communities. People with healthy brains are essential to navigate increasingly complex systems. Policies and investments that improve brain health and hence citizens' cognitive functions and boost brain performance can increase productivity, stimulate greater creativity and economic dynamism, utilise often underdeveloped intellectual resources, afford social cohesion, and create a more resilient, adaptable and sustainability-engaged population. [ABSTRACT FROM AUTHOR]