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ObjectiveThe effect of ghrelin on glucose metabolism is still controversial. This study aims to investigate the effects of long-term application of acyl ghrelin (AG) and des-acyl ghrelin (DAG) on insulin resistance and serum inflammatory factor levels by establishing a mouse model of obesity, induced by a high-fat diet.MethodsThirty two male C57BL/6 mice were randomly divided into 4 groups, 8 in each group. Except for the control group, the high fat diet group (HFD), HFD+AG group and HFD+DAG group were given a high-fat diet to induce obesity in mice. Control group: standard feed and an intraperitoneal injection of 10mL isotonic saline were given every day. HFD: high-fat feed and an intraperitoneal injection of 10mL isotonic saline were given every day. HFD+AG group: high-fat diet was fed with 0.8mg AG; HFD+DAG group: high-fat diet was fed with 0.8mg DAG. Intraperitoneal glucose tolerance test (IPGTT) was performed 16 weeks later. The blood glucose was collected from the tail veins at 0min, 30min, 60min and 120min after injection, respectively, the fluctuation curve was drawn, the area under the curve was calculated, and then the epididymal fat index was weighted. Fasting insulin, interleukin 6 (IL6) and TNFα levels were measured by enzyme-linked immunosorbent assay (ELISA). Then the insulin resistance index (HOMA IR) was compared.ResultsAfter 6 weeks of feeding, the weight of the mice in HFD was significantly higher than that of the control group (P<0.05). After 14 and 12 weeks of administration, the mice in the HFD+AG group and the HFD+DAG group had a significant weight loss (P<0.05). The fat mass of the epididymis in the HFD+DAG group [(0.92±0.32)g] was significantly lower than that of the HFD group [(1.08±0.11)g] (P<0.05); the fasting insulin level was significantly lower, too (P<0.05). The insulin resistance index (4.94±1.27, 4.08±1.35), IL6 [(34.82±6.23), (36.90±5.27)pg/mL] and TNFα levels [(73.01±7.75), (69.39±8.43)pg/mL] in the HFD+AG group and HFD+DAG group were significantly lower than those in the HFD group [(81.70±7.53), (45.85±6.41) pg/mL, (81.70±7.53)pg/mL], with statistically significant differences (P<0.05). The serum levels of IL 6 and TNFα in the HFD group were significantly lower than those in the control group (P<0.05).ConclusionLong-term application of AG and DAG could improve the insulin resistance and reduce the inflammation level of the mice induced by a high-fat diet. DAG can also decrease the visceral fat in mice.
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Vitamin B12 (VitB12) is one of the essential vitamins in humans and is involved in DNA synthesis and cellular metabolism. Many studies have shown that the lack of VitB12 is closely related to the occurrence and development of diabetes and its complications. Therefore, regular testing and reasonable supplementation of VitB12 can help prevent diabetes complications. The article reviews the relationship between VitB12 and diabetes as well as the application of VitB12 in diabetic patients.
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<p><b>OBJECTIVE</b>To investigate the expression of HBx and COX-2 in hepatitis B virus-related hepatocellular carcinoma, and Its correlation with microangiogenesis and metastasis, and possible mechanism.</p><p><b>METHODS</b>Immunohistochemistry was used to detect the expression of hepatitis B virus X, cyclooxygenase-2 and CD34 in hepatitis B virus related hepatic carcinoma and 22 non-HBV related hepatic carcinoma tissues. The expression of hepatitis B virus x protein and cyclooxygenase-2 in hepatitis B virus-related hepatocellular carcinoma correlated with microangiogenesis and metastasis was tested by Spearman correlation analysis. The expression of COX-2 in HepG2-X was detected by Western blot and RT-PCR. PGE2 was detected by ELISA in clear supernatant liquid of HepG2-X. Trypan blue exclusion was performed to examine the inhibitory effects of COX-2 selective inhibitor (celecoxib).</p><p><b>RESULTS</b>In Hepatitis B carcinoma tissue, HBx and COX-2 were expressed at high level. The positive rate of COX-2 expression was 88.87% (55/62) in HBx positive expression group, which was significantly higher than that of the positive expression 31.82% (7/22, x2=27.188, P<0.01) in HBx negative expression group and 40.91% (9/22, x2=20.453, P<0.01) in non-HBV related hepatic carcinoma tissues, but it had no statistical difference (x2=0.393, P=0.531) between the HBx negative expression group and non-HBV related hepatic carcinoma tissue group. The expressions of HBx and COX-2 in metastasis group were higher than that in non-metastasis group (P<0.01), MVD in HBx or COX-2 positive expression group was significantly higher than that in negative expression group and non-HBV related hepatic carcinoma tissues (P is less than 0.01). MVD with metastasis was higher than that without metastasis (P<0.01) and MVD with portal vein invasion was higher than that without invasion (P<0.05). Spearman correlation analysis showed that the expression of COX-2 was significantly correlated with the expression of HBx (Rs=0.568, P<0.01). Celecoxib suppressed the growth of both cells in a dose-dependent manner. HepG2-X was significantly susceptible to celecoxib as compared to the HepG2-PC cells. COX-2 protein and mRNA were upregulated in HepG2-X cells than in HepG2-PC. Moreover, PGE2 was upregulated in clear supernatant liquid of HepG2-X than in HepG2-PC.</p><p><b>CONCLUSION</b>The expressions of HBx and COX-2 were higher in HBV-related hepatocellular carcinoma. COX-2 was significantly correlated with HBx in HCC and it could be a key factor involved in HBx contributed hepatocellular carcinoma's microangiogenesis and metastasis. The possible mechanism of the dual effects might be through HBx, COX-2 and PGE2 pathways in infiltration involved metastasis and microangiogenesis involved metastasis.</p>