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《糖尿病学杂志》2005年第09期

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new clinical syndromes, new scientific insights, and new therapy
differentiation of human liver-derived, insulin-producing cells toward the -cell phenotype
essential role for membrane lipid rafts in interleukin-1ecinduced nitric oxide release from insulin-secreting cells
conditional expression demonstrates the role of the homeodomain transcription factor pdx1 in maintenance and regeneration of -cells in the adult pancreas
combination therapy with epidermal growth factor and gastrin increases -cell mass and reverses hyperglycemia in diabetic nod mice
exposure to chronic high glucose induces -cell apoptosis through decreased interaction of glucokinase with mitochondria
matrix metalloproteinases contribute to insulin insufficiency in zucker diabetic fatty rats
glucagon-like peptide 1 regulates sequential and compound exocytosis in pancreatic islet -cells
transgenic mouse overexpressing syntaxin-1a as a diabetes model
chronic hyperglycemia, independent of plasma lipid levels, is sufficient for the loss of -cell differentiation and secretory function in the db/db mouse model of di..
marked increase in white adipose tissue blood perfusion in the type 2 diabetic gk rat
cardiac-specific overexpression of peroxisome proliferatorecactivated receptor- causes insulin resistance in heart and liver
experimental diabetes attenuates cerebral corticalecevoked forelimb motor responses
adiponectin is lower among african americans and is independently related to insulin sensitivity in children and adolescents
activation of peripheral blood cd14+ monocytes occurs in diabetes
characterization of susceptibility of inbred mouse strains to diabetic nephropathy
type 2 diabetes causes remodeling of cerebrovasculature via differential regulation of matrix metalloproteinases and collagen synthesis
atp and sulfonylurea sensitivity of mutant atp-sensitive k+ channels in neonatal diabetes
genome-wide linkage analyses of type 2 diabetes in mexican americans
variation in the enos gene modifies the association between total energy expenditure and glucose intolerance
co-occurrence of two partially inactivating polymorphisms of mc3r is associated with pediatric-onset obesity
haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction
acute bidirectional manipulation of muscle glucose uptake by in vivo electrotransfer of constructs targeting glucose transporter genes
the functional q84r polymorphism of mammalian tribbles homolog trb3 is associated with insulin resistance and related cardiovascular risk in caucasians from italy
ins vntr class genotype and indexes of body size and obesity
lack of association of pax4 gene with type 1 diabetes in the finnish and hungarian populations
colocalization of mouse autoimmune diabetes loci idd21.1 and idd21.2 with iddm6 (human) and iddm3 (rat)
spillover of dietary fatty acids and use of serum nonesterified fatty acids for the synthesis of vldl-triacylglycerol under two different feeding regimens
overactivation of s6 kinase 1 as a cause of human insulin resistance during increased amino acid availability
expression of mfn2, the charcot-marie-tooth neuropathy type 2a gene, in human skeletal muscle
increased dietary substrate delivery alters hepatic fatty acid recycling in healthy men
changes of adiponectin oligomer composition by moderate weight reduction
increased fat mass compensates for insulin resistance in abdominal obesity and type 2 diabetes
novel leptin receptor mutation in nod/ltj mice suppresses type 1 diabetes progression
rosiglitazone improves myocardial glucose uptake in patients with type 2 diabetes and coronary artery disease
the x-linked inhibitor of apoptosis protein enhances survival of murine islet allografts
xiap overexpression in human islets prevents early posttransplant apoptosis and reduces the islet mass needed to treat diabetes
interferon- as a mediator of polyinosinic:polycytidylic acidecinduced type 1 diabetes
lew.1wr1 rats develop autoimmune diabetes spontaneously and in response to environmental perturbation
very slow turnover of -cells in aged adult mice
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