Ups and Downs in Finance, Ups without Downs in Inequality

The upswing in finance over the past several decades has led to rising inequality, but do downswings in finance lead to a symmetric decline in inequality? In this paper, we analyze the asymmetry of the effect of ups and downs in financial markets, as well as the effect of increased capital requirements and the bonus cap on national earnings in- equality. We use administrative employer–employee linked data on earnings from 1990 to 2017 for twelve countries. Additionally, we use data on earnings from bank reports, from 2009 to 2017 in thirteen European countries. We find a strong asymmetry in the effects of financial ups and downs on earnings inequality, a mitigating effect of rising capital requirements on the contribution of finance to inequality, and a restructuring ef- fect of the bonus cap for the earnings of financiers, while neither policy affects absolute levels of earnings inequality.La hausse de la finance au cours des dernières décennies a entraîné une hausse des inégalités, mais les ralentissements de la finance entraînent-ils une baisse symétrique des inégalités? Dans cet article, nous examinons l'asymétrie de l'effet des hausses et des ralentissements des marchés financiers, ainsi que l'effet de l'augmentation des exi- gences en matière de capital et du plafonnement des primes sur l'inégalité des salaires nationaux. Nous utilisons des données administratives couplées employeur-employé sur les salaires de 1990 à 2017 pour douze pays. De plus, nous employons des données sur les salaires provenant des rapports bancaires, de 2009 à 2017, dans 13 pays euro- péens. Nous constatons une forte asymétrie dans les effets des hausses et des ralentis- sements financières sur l'inégalité des salaires, un effet de mitigation de l'augmentation des exigences de capitalisation sur la contribution de la finance à l'inégalité, et un effet de restructuration du plafonnement des primes pour les salaires des financiers, alors qu'aucune des deux mesures n'affecte les niveaux absolus d'inégalité des salaires.iv MaxPo Discussion Paper 21/2 1 Introduction 2 Data Administrative employer–employee linked data World Bank GFDD database European bank reports 3 The contribution of financiers’ earnings to inequality and its asymmetry in upswings and downswings Less finance, less inequality? The asymmetry of the redistribution of earnings through financialization 4 Finance, regulation, and inequality Capital requirements and inequality The bonus cap 5 Conclusion Appendices A1 Data description A2 Supplementary tables and figures Reference

The effect of acute exercise on glycogen synthesis rate in obese subjects studied by 13C MRS

In obesity, insulin-stimulated glucose uptake in skeletal muscle is decreased. We investigated whether the stimulatory effect of acute exercise on glucose uptake and subsequent glycogen synthesis was normal. The study was performed on 18 healthy volunteers, 9 obese (BMI = 32.6 ± 1.2 kg/m2, mean ± SEM) and 9 lean (BMI = 22.0 ± 0.9 kg/m2), matched for age and gender. All participants underwent a euglycemic hyperinsulinemic clamp, showing reduced glucose uptake in the obese group (P = 0.01), during which they performed a short intense local exercise (single-legged toe lifting). Dynamic glucose incorporation into glycogen in the gastrocnemius muscle before and after exercise was assessed by 13C magnetic resonance spectroscopy combined with infusion of [1-13C]glucose. Blood flow was measured to investigate its potential contribution to glucose uptake. Before exercise, glycogen synthesis rate tended to be lower in obese subjects compared with lean (78 ± 14 vs. 132 ± 24 μmol/kg muscle/min; P = 0.07). Exercise induced highly significant rises in glycogen synthesis rates in both groups, but the increase in obese subjects was reduced compared with lean (112 ± 15 vs. 186 ± 27 μmol/kg muscle/min; P = 0.03), although the relative increase was similar (184 ± 35 vs. 202 ± 51%; P = 0.78). After exercise, blood flow increased equally in both groups, without a temporal relationship with the rate of glycogen synthesis. In conclusion, this study shows a stimulatory effect of a short bout of acute exercise on insulin-induced glycogen synthesis rate that is reduced in absolute values but similar in percentages in obese subjects. These results suggest a shared pathway between insulin- and exercise-induced glucose uptake and subsequent glycogen synthesis

Exercise training with dietary counselling increases mitochondrial chaperone expression in middle-aged subjects with impaired glucose tolerance

<p>Abstract</p> <p>Background</p> <p>Insulin resistance and diabetes are associated with increased oxidative stress and impairment of cellular defence systems. Our purpose was to investigate the interaction between glucose metabolism, antioxidative capacity and heat shock protein (HSP) defence in different skeletal muscle phenotypes among middle-aged obese subjects during a long-term exercise and dietary intervention. As a sub-study of the Finnish Diabetes Prevention Study (DPS), 22 persons with impaired glucose tolerance (IGT) taking part in the intervention volunteered to give samples from the <it>vastus lateralis </it>muscle. Subjects were divided into two sub-groups (IGTslow and IGTfast) on the basis of their baseline myosin heavy chain profile. Glucose metabolism, oxidative stress and HSP expressions were measured before and after the 2-year intervention.</p> <p>Results</p> <p>Exercise training, combined with dietary counselling, increased the expression of mitochondrial chaperones HSP60 and glucose-regulated protein 75 (GRP75) in the <it>vastus lateralis </it>muscle in the IGTslow group and that of HSP60 in the IGTfast group. In cytoplasmic chaperones HSP72 or HSP90 no changes took place. In the IGTslow group, a significant positive correlation between the increased muscle content of HSP60 and the oxygen radical absorbing capacity values and, in the IGTfast group, between the improved VO_2maxvalue and the increased protein expression of GRP75 were found. Serum uric acid concentrations decreased in both sub-groups and serum protein carbonyl concentrations decreased in the IGTfast group.</p> <p>Conclusion</p> <p>The 2-year intervention up-regulated mitochondrial HSP expressions in middle-aged subjects with impaired glucose tolerance. These improvements, however, were not correlated directly with enhanced glucose tolerance.</p

Socioeconomic variation in child educational and socioeconomic attainment after parental death in Sweden

In this study we use Swedish population register data to examine whether parental death differentially affects educational and occupational attainment according to the socioeconomic status of the parent who dies, and the socioeconomic status of the surviving parent and extended kin. That is, we examine whether parental death has an equalizing or exacerbating effect on offspring socioeconomic attainment, and also whether the socioeconomic status of the rest of the family plays a meaningful role in compensating for parental death. Using data on cohorts born 1973 to 1982 we examine five different outcomes, which are grade point average (GPA) at age 16 in high school, the transition from lower to upper-secondary education, the transition to tertiary education, overall educational attainment, and occupational status by age 30. We match families based upon antemortem parental socioeconomic trajectories. Overall we find mixed results in our between-family regression analyses adjusting for observables, with inconsistent evidence suggesting that losing a parent with very high socioeconomic resources is worse, and some evidence for a protective effect if the socioeconomic resources of the surviving parent and extended family members are at the top of the distribution. Using sibling fixed effects models that adjust for unobservable factors shared within the family, we see zero results for moderation by parents&rsquo; SES, but find consistent evidence that it is worse to lose a father at a younger age if grandparents have higher ranked occupations. We discuss possible interpretations of our findings

Decreased Thioredoxin-1 and Increased HSP90 Expression in Skeletal Muscle in Subjects with Type 2 Diabetes or Impaired Glucose Tolerance

In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) ( = 10) were compared with subjects with impaired glucose tolerance (IGT) ( = 8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower ( = 0.031) and HSP90 was 380% higher ( &lt; 0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research