RESUMO
There is a growing interest in the role of glucagon in type 2 diabetes mellitus (T2DM). Glucagon and insulin regulate glucose and lipid metabolism. Metabolic syndrome is an important risk factor for cardiovascular disease in patients with T2DM. We investigated the association between glucagon to insulin ratio and metabolic syndrome in patients with T2DM. This is a cross-sectional study involving 317 people with type 2 diabetes. Glucagon and insulin levels were measured in a fasted state and 30 min after ingesting a standard mixed meal. The Criteria of the International Diabetes Federation defined metabolic syndrome. Two hundred nineteen (69%) of the subjects had metabolic syndrome. The fasting glucagon to insulin ratio was significantly lower in patients with metabolic syndrome (14.0 ± 9.7 vs. 17.3 ± 10.3, p < 0.05). The fasting glucagon to insulin ratio was significantly lowered as the number of metabolic syndrome components increased. In hierarchical logistic regression analysis, the fasting glucagon to insulin ratio significantly contributed to metabolic syndrome even after adjusting for other covariates. The fasting glucagon to insulin ratio is inversely associated with metabolic syndrome in patients with type 2 diabetes. This suggests that glucagon-targeted therapeutics may reduce cardiovascular risk by improving metabolic syndrome.
RESUMO
Nephrogenic systemic fibrosis (NSF) is a progressive systemic fibrosing disease that may occur after gadolinium contrast exposure. It can lead to severe complications and even death. NSF is highly prevalent among patients with advanced chronic kidney disease (CKD). In this report, however, we describe the case of a patient with NSF that occurred during early CKD. A 65-year-old man with stage 3a CKD was transferred to our hospital because of lower extremity edema. The medical history revealed that he was exposed to gadolinium 185 days earlier, and the result of his tibial skin biopsy was consistent with NSF. The patient underwent a combined therapy with ultraviolet-A1 phototherapy and methotrexate and steroid therapy for 6 months. The combined therapy stopped the systemic progression of NSF.
Assuntos
Dermopatia Fibrosante Nefrogênica/diagnóstico , Insuficiência Renal Crônica/patologia , Idoso , Meios de Contraste/efeitos adversos , Meios de Contraste/química , Fármacos Dermatológicos/uso terapêutico , Progressão da Doença , Gadolínio/química , Taxa de Filtração Glomerular , Humanos , Imageamento por Ressonância Magnética , Masculino , Metotrexato/uso terapêutico , Dermopatia Fibrosante Nefrogênica/etiologia , Dermopatia Fibrosante Nefrogênica/terapia , Índice de Gravidade de Doença , Pele/patologia , Terapia UltravioletaRESUMO
Vibrio vulnificus is an opportunistic pathogen that causes septicemia in humans. To identify the genes associated with its pathogenicity, in vivo expression technology (IVET) was used to select genes specifically expressed in a host, yet not significantly in vitro. Random lacZ-fusions in the genome of V. vulnificus strain MO6-24/O were constructed using an IVET vector, pSG3, which is a suicide vector containing promoterless-aph and -lacZ as reporter genes. A total of approximately 18,000 resulting library clones were then intraperitoneally injected into BALB/c mice using a colony forming unit (CFU) of 1.6 x 10(6). Two hours after infection, kanamycin was administered at 200 microg per gram of mouse weight. After two selection cycles, 11 genes were eventually isolated, which were expressed only in the host. Among these genes, VV20781 and VV21007 exhibiting a homology to a hemagglutinin gene and tolC, respectively, were selected based on having the highest frequency. When compared to wild-type cells, mutants with lesions in these genes showed no difference in the rate of growth rate, yet a significant decrease in cytotoxicity and the capability to form a biofilm.
