ObjectiveTo assess the prevalence of diabetes and its risk factors.DesignPopulation based, cross sectional study.Setting31 provinces in mainland China with nationally representative cross sectional data from 2015 to 2017.Participants75 880 participants aged 18 and older—a nationally representative sample of the mainland Chinese population.Main outcome measuresPrevalence of diabetes among adults living in China, and the prevalence by sex, regions, and ethnic groups, estimated by the 2018 American Diabetes Association (ADA) and the World Health Organization diagnostic criteria. Demographic characteristics, lifestyle, and history of disease were recorded by participants on a questionnaire. Anthropometric and clinical assessments were made of serum concentrations of fasting plasma glucose (one measurement), two hour plasma glucose, and glycated haemoglobin (HbA1c).ResultsThe weighted prevalence of total diabetes (n=9772), self-reported diabetes (n=4464), newly diagnosed diabetes (n=5308), and prediabetes (n=27 230) diagnosed by the ADA criteria were 12.8% (95% confidence interval 12.0% to 13.6%), 6.0% (5.4% to 6.7%), 6.8% (6.1% to 7.4%), and 35.2% (33.5% to 37.0%), respectively, among adults living in China. The weighted prevalence of total diabetes was higher among adults aged 50 and older and among men. The prevalence of total diabetes in 31 provinces ranged from 6.2% in Guizhou to 19.9% in Inner Mongolia. Han ethnicity had the highest prevalence of diabetes (12.8%) and Hui ethnicity had the lowest (6.3%) among five investigated ethnicities. The weighted prevalence of total diabetes (n=8385) using the WHO criteria was 11.2% (95% confidence interval 10.5% to 11.9%).ConclusionThe prevalence of diabetes has increased slightly from 2007 to 2017 among adults living in China. The findings indicate that diabetes is an important public health problem in China.

Enhancing skeletal muscle growth is crucial for animal agriculture because skeletal muscle provides meat for human consumption. An increasing body of evidence shows that the level of maternal nutrition alters fetal skeletal muscle development, with long-term effects on offspring growth and performance. Fetal skeletal muscle development mainly involves myogenesis (i.e., muscle cell development), but also involves adipogenesis (i.e., adipocyte development) and fibrogenesis (i.e., fibroblast development). These tissues in fetal muscle are mainly derived from mesenchymal stem cells (MSC). Shifting the commitment of MSC from myogenesis to adipogenesis increases intramuscular fat (i.e., marbling), improving the quality grade of meats. Strong experimental evidence indicates that Wingless and Int (Wnt)/beta-catenin signaling regulates MSC differentiation. Upregulation of Wnt/beta-catenin promotes myogenesis, and downregulation enhances adipogenesis. A lack of nutrients in early to midgestation reduces the formation of secondary muscle fibers in ruminant animals. Nutrient deficiency during mid- to late gestation decreases the number of intramuscular adipocytes and muscle fiber sizes. Knowledge of this regulatory mechanism will allow the development of strategies to enhance muscle growth and marbling in offspring, especially in the setting of nutrient deficiency.

Maternal nutrient restriction (NR) affects fetal development with long-term consequences on postnatal health of offspring, including predisposition to obesity and diabetes. Most studies have been conducted in fetuses in late gestation, and little information is available on the persistent impact of NR from early to mid-gestation on properties of offspring skeletal muscle, which was the aim of this study. Pregnant ewes were subjected to 50% NR from day 28-78 of gestation and allowed to deliver. The longissimus dorsi muscle was sampled from 8-month-old offspring. Maternal NR during early to mid-gestation decreased the number of myofibres in the offspring and increased the ratio of myosin IIb to other isoforms by 17.6 ± 4.9% (P < 0.05) compared with offspring of ad libitum fed ewes. Activity of carnitine palmitoyltransferase-1, a key enzyme controlling fatty acid oxidation, was reduced by 24.7 ± 4.5% (P < 0.05) in skeletal muscle of offspring of NR ewes and would contribute to increased fat accumulation observed in offspring of NR ewes. Intramuscular triglyceride content (IMTG) was increased in skeletal muscle of NR lambs, a finding which may be linked to predisposition to diabetes in offspring of NR mothers, since enhanced IMTG predisposes to insulin resistance in skeletal muscle. Proteomic analysis by two-dimensional gel electrophoresis demonstrated downregulation of several catabolic enzymes in 8-month-old offspring of NR ewes. These data demonstrate that the early to mid-gestation period is important for skeletal muscle development. Impaired muscle development during this stage of gestation affects the number and composition of fibres in offspring which may lead to long-term physiological consequences, including predisposition to obesity and diabetes.

␤cyto-Actin and ␥cyto-actin are ubiquitous proteins thought to be essential building blocks of the cytoskeleton in all non-muscle cells. Despite this widely held supposition, we show that ␥cyto-actin null mice (Actg1 ؊/؊ ) are viable. However, they suffer increased mortality and show progressive hearing loss during adulthood despite compensatory up-regulation of ␤cyto-actin. The surprising viability and normal hearing of young Actg1 ؊/؊ mice means that ␤cyto-actin can likely build all essential non-muscle actin-based cytoskeletal structures including mechanosensory stereocilia of hair cells that are necessary for hearing. Although ␥cyto-actin-deficient stereocilia form normally, we found that they cannot maintain the integrity of the stereocilia actin core. In the wild-type, ␥cyto-actin localizes along the length of stereocilia but re-distributes to sites of F-actin core disruptions resulting from animal exposure to damaging noise. In Actg1 ؊/؊ stereocilia similar disruptions are observed even without noise exposure. We conclude that ␥cyto-actin is required for reinforcement and long-term stability of F-actin-based structures but is not an essential building block of the developing cytoskeleton.actin ͉ cytoskeleton ͉ hearing T here are six genes encoding six vertebrate actins that are classified according to where they are predominately expressed. ␣ skeletal -Actin, ␣ smooth -actin, ␣ cardiac -actin, and ␥ smoothactin are primarily found in muscle cells, whereas cytoplasmic ␤ cyto -actin and ␥ cyto -actin are ubiquitously and highly expressed in non-muscle cells, as reviewed elsewhere (1). Athough ␤ cytoactin and ␥ cyto -actin differ at only four biochemically similar amino acid residues in their N-termini, several lines of evidence suggest that each protein is functionally distinct. The amino acid sequences of ␤ cyto -and ␥ cyto -actin are each exactly conserved among avian and mammalian species. In addition, ␤ cyto -and ␥ cyto -actin proteins are differentially localized (2-5) and posttranslationally modified (6). Finally, although dominant missense mutations in ACTB encoding ␤ cyto -actin are associated with syndromic phenotypes including severe developmental malformations and bilateral deafness (7), humans carrying a variety of dominant missense mutations in ACTG1 develop postlingual nonsyndromic progressive hearing loss (DFNA20, OMIM 604717) (8-11).␥ cyto -Actin is widely expressed in the inner ear sensory epithelial cells on which mammalian hearing depends. These cells are organized in rows along the cochlea length: one row of inner hair cells (IHCs) and three rows of outer hair cells (OHCs) (Fig. 2A). IHCs function as auditory receptors, converting sound energy into neuronal signals, whereas OHCs enhance sensitivity to sound stimuli, as reviewed elsewhere (12). The apical surface of a hair cell is topped with actin-rich microvilli-derived protrusions termed stereocilia, which deflect in response to sound stimuli, initiating mechanoelectrical transduction (Fig. 2B). ␤ cyto -and ␥ cyto -Actin are both thou...

Synaptic vesicle (SV) pools must maintain a functional repertoire of proteins to efficiently release neurotransmitter. The accumulation of old or damaged proteins on SV membranes is linked to synaptic dysfunction and neurodegeneration. However, despite the importance of SV protein turnover for neuronal health, the molecular mechanisms underlying this process are largely unknown. Here, we have used dissociated rat hippocampal neurons to investigate the pathway for SV protein degradation. We find that neuronal activity drives the degradation of a subset of SV proteins and that the endosomal sorting complex required for transport (ESCRT) machinery and SVassociated GTPase Rab35 are key elements of this use-dependent degradative pathway. Specifically, neuronal activity induces Rab35 activation and binding to the ESCRT-0 protein Hrs, which we have identified as a novel Rab35 effector. These actions recruit the downstream ESCRT machinery to SV pools, thereby initiating SV protein degradation via the ESCRT pathway. Our findings show that the Rab35/ESCRT pathway facilitates the activity-dependent removal of specific proteins from SV pools, thereby maintaining presynaptic protein homeostasis.