Gestational diabetes mellitus in Cameroon: prevalence, risk factors and screening strategies

Copyright \ua9 2024 Sobngwi, Sobngwi-Tambekou, Katte, Echouffo-Tcheugui, Balti, Kengne, Fezeu, Ditah, Tchatchoua, Dehayem, Unwin, Rankin, Mbanya and Bell.Background: The burden of gestational diabetes (GDM) and the optimal screening strategies in African populations are yet to be determined. We assessed the prevalence of GDM and the performance of various screening tests in a Cameroonian population. Methods: We carried out a cross-sectional study involving the screening of 983 women at 24-28 weeks of pregnancy for GDM using serial tests, including fasting plasma (FPG), random blood glucose (RBG), a 1-hour 50g glucose challenge test (GCT), and standard 2-hour oral glucose tolerance test (OGTT). GDM was defined using the World Health Organization (WHO 1999), International Association of Diabetes and Pregnancy Special Group (IADPSG 2010), and National Institute for Health Care Excellence (NICE 2015) criteria. GDM correlates were assessed using logistic regressions, and c-statistics were used to assess the performance of screening strategies. Findings: GDM prevalence was 5\ub79%, 17\ub77%, and 11\ub70% using WHO, IADPSG, and NICE criteria, respectively. Previous stillbirth [odds ratio: 3\ub714, 95%CI: 1\ub727-7\ub776)] was the main correlate of GDM. The optimal cut-points to diagnose WHO-defined GDM were 5\ub79 mmol/L for RPG (c-statistic 0\ub762) and 7\ub71 mmol/L for 1-hour 50g GCT (c-statistic 0\ub776). The same cut-off value for RPG was applicable for IADPSG-diagnosed GDM while the threshold was 6\ub75 mmol/L (c-statistic 0\ub761) for NICE-diagnosed GDM. The optimal cut-off of 1-hour 50g GCT was similar for IADPSG and NICE-diagnosed GDM. WHO-defined GDM was always confirmed by another diagnosis strategy while IADPSG and GCT independently identified at least 66\ub79 and 41\ub70% of the cases. Interpretation: GDM is common among Cameroonian women. Effective detection of GDM in under-resourced settings may require simpler algorithms including the initial use of FPG, which could substantially increase screening yield

Oxygen Consumption Can Regulate the Growth of Tumors, a New Perspective on the Warburg Effect

The unique metabolism of tumors was described many years ago by Otto Warburg, who identified tumor cells with increased glycolysis and decreased mitochondrial activity. However, "aerobic glycolysis" generates fewer ATP per glucose molecule than mitochondrial oxidative phosphorylation, so in terms of energy production, it is unclear how increasing a less efficient process provides tumors with a growth advantage.We carried out a screen for loss of genetic elements in pancreatic tumor cells that accelerated their growth as tumors, and identified mitochondrial ribosomal protein L28 (MRPL28). Knockdown of MRPL28 in these cells decreased mitochondrial activity, and increased glycolysis, but paradoxically, decreased cellular growth in vitro. Following Warburg's observations, this mutation causes decreased mitochondrial function, compensatory increase in glycolysis and accelerated growth in vivo. Likewise, knockdown of either mitochondrial ribosomal protein L12 (MRPL12) or cytochrome oxidase had a similar effect. Conversely, expression of the mitochondrial uncoupling protein 1 (UCP1) increased oxygen consumption and decreased tumor growth. Finally, treatment of tumor bearing animals with dichloroacetate (DCA) increased pyruvate consumption in the mitochondria, increased total oxygen consumption, increased tumor hypoxia and slowed tumor growth.We interpret these findings to show that non-oncogenic genetic changes that alter mitochondrial metabolism can regulate tumor growth through modulation of the consumption of oxygen, which appears to be a rate limiting substrate for tumor proliferation