Updates of Nursing Practice Guideline for Enteral Nutrition / 임상간호연구

Purpose@#The purpose of this study was to update the previously developed nursing practice guideline for enteral nutrition (EN). @*Methods@#The guideline update was done in 22 steps using standardized methodology for nursing practice guidelines. @*Results@#The updated EN guideline consisted of 16 domains and 228 recommendations. The domains and number of recommendations in each domain were for IDSA (Infectious Diseases Society of America): 8 on general instruction, 9 on general instruction for special nutrition, 9 on general instruction for EN, 3 on assessment of EN, 10 on access to EN, 18 on EN device insertion, 16 on selection and preparation of nutritional supplements, 46 on administration and stopping EN, 22 on maintenance and management of EN, 9 on monitoring EN, 16 on prevention and management of complications of EN, 18 on medication administration, 20 on EN in various situations, 20 on prevention of errors, 1 on nursing education, and 3 on nursing documentation. For the levels of evidence, there were 9.7% for level I, 13.1% for level II, 62.5% for level III and 1.1% for GRADE (Grading of Recommendations Assessment, Development and Evaluation): 3.3% for low, 0.8% for moderate, 9.3% for very low. A total of 133 recommendations were newly developed and 10 previous recommendations were modified. @*Conclusion@#This updated EN nursing practice guideline can be used to enhance evidence-based practice in fundamentals of nursing practice and it should be disseminated to nurses nationwide in order to improve the efficiency of EN practice.

Nutrition Support Nurse: Roles and Tasks

Nutrition care is important for patients’ well-being. With legislation for reimbursement for nutrition support team activities from the Korea Ministry of Health and Welfare, this has increased the importance of nurses’ role in nutrition. Nutrition support nurses (NSNs) focus on the optimization of nutritional health and prevention of nutrition-related illness and injury. NSN performs as an advanced practice nurse, a core member of a nutrition support team, an educator or consultant, a policy maker in nutrition care, and a researcher or a member of quality improvement. NSNs should develop their core competency to fulfill their roles in nutrition care and the need to participate in qualified nutrition support education programs. Further, the tasks and duties of NSNs should be specifically identified so that NSNs can fulfill their roles.

Ginsenoside Re lowers blood glucose and lipid levels via activation of AMP-activated protein kinase in HepG2 cells and high-fat diet fed mice.

Ginsenoside Re is a protopanaxatriol-type saponin isolated from Panax ginseng berry. Although anti-diabetic and anti-hyperlipidemic effects of Re have been reported by several groups, its mechanism of action is largely unknown until now. Here, we examine anti-diabetic and anti-hyperlipidemic activities of Re and action mechanism(s) in human HepG2 hepatocytes and high-fat diet fed C57BL/6J mice. Re suppresses the hepatic glucose production via induction of orphan nuclear receptor small heterodimer partner (SHP), and inhibits lipogenesis via suppression of sterol regulatory element binding protein-1c (SREBP-1c) and its target gene [fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD1)] transcription. These effects were mediated through activation of AMP-activated protein kinase (AMPK), and abolished when HepG2 cells were treated with an AMPK inhibitor, Compound C. C57BL/6J mice were randomly divided into five groups: regular diet fed group (RD), high-fat diet fed group (HFD) and the HFD plus Re (5, 10, 20 mg/kg) groups. Re treatment groups were fed a high-fat diet for 6 weeks, and then orally administered Re once a day for 3 weeks. The in vitro results are likely to hold true in an in vivo experiment, as Re markedly lowered blood glucose and triglyceride levels and protected against hepatic steatosis in high-fat diet fed C57BL/6J mice. In conclusion, the current study suggest that ginsenoside Re improves hyperglycemia and hyperlipidemia through activation of AMPK, and confers beneficial effects on type 2 diabetic patients with insulin resistance and dyslipidemia.

Ginsenoside Rd stimulates the differentiation and mineralization of osteoblastic MC3T3-E1 cells by activating AMP-activated protein kinase via the BMP-2 signaling pathway.

As part of our search for biologically active anti-osteoporotic agents that enhance the differentiation and mineralization of osteoblastic MC3T3-E1 cells, we identified the ginsenoside Rd as the most active compound among ginsenosides. In this study, we showed that Rd stimulates osteoblastic differentiation and mineralization, manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and von Kossa/Alizarin Red staining, respectively. Rd induces the mRNA expression of bone morphogenetic protein-2 (BMP-2) and the secretion of the corresponding protein into media in a concentration-dependent manner. The mRNA expression and enzyme activity of alkaline phosphatase (ALP) were suppressed when MC3T3-E1 cells were exposed to noggin, a BMP-2 antagonist. The level of phosphorylated AMP-activated protein kinase (pAMPK) protein was also up-regulated by Rd in a time- and concentration-dependent manner. Rd-induced ALP activity, mineralization, and BMP-2 production were all inhibited by either Ara-A (AMPK inhibitor) or siRNA targeting AMPK. In addition, we investigated whether Rd-induced BMP-2 transduces signals through the Smad signaling pathways. Rd induced a significant level of phosphorylation of Smad1/5, and this effect was blocked when the cells were transfected with siRNA targeting Smad4, indicating that Smad1/5 must form complex with Smad4 to translocate into the nucleus and regulate the transcription of osteogenic genes. In summary, these results indicate that Rd induces the differentiation and mineralization of MC3T3-E1 cells through the activation of the AMPK/BMP-2/Smad signaling pathways. These findings provide a molecular basis for the osteogenic effect of Rd in MC3T3-E1 cells.

Ginsenoside Rg2 induces orphan nuclear receptor SHP gene expression and inactivates GSK3ß via AMP-activated protein kinase to inhibit hepatic glucose production in HepG2 cells.

Panax ginseng is known to have anti-diabetic activity, but the active ingredients have not been fully explored yet. Here, we test whether ginsenoside Rg2 has an inhibitory effect on hepatic glucose production and determine its mechanism of action. Rg2 significantly inhibits hepatic glucose production and induces phosphorylations of liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK) and glycogen synthase kinase 3ß (GSK3ß) in time- and concentration-dependent manners in human HepG2 hepatoma cells, and these effects were abolished in the presence of compound C, a selective AMPK inhibitor. In addition, phosphorylated form of cAMP-response element-binding protein (CREB), a key transcription factor for hepatic gluconeogenesis, was decreased in time- and concentration-dependent manners. Next, gene expression of orphan nuclear receptor small heterodimer partner (SHP) was also examined. Rg2 markedly enhanced the gene expression of SHP and its direct interaction with CREB, which results in disruption of CREB·CRTC2 complex. Consequently, expressions of relevant genes such as peroxisome proliferation-activated receptor γ coactivator-1α (PGC-1α), phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) were all significantly suppressed and these effects were also reversed in the presence of compound C. In conclusion, our results propose that ginsenoside Rg2 suppresses the hepatic glucose production via AMPK-induced phosphorylation of GSK3ß and induction of SHP gene expression. Further studies are warranted to elucidate a therapeutic potential of Rg2 for type 2 diabetic patients.

Ginsenoside Rh2(S) induces the differentiation and mineralization of osteoblastic MC3T3-E1 cells through activation of PKD and p38 MAPK pathways.

As part of the search for biologically active anti-osteoporotic agents that enhance differentiation and mineralization of osteoblastic MC3T3-E1 cells, we identified the ginsenoside Rh2(S), which is an active component in ginseng. Rh2(S) stimulates osteoblastic differentiation and mineralization, as manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and Alizarin Red staining, respectively. Rh2(S) activates p38 mitogen-activated protein kinase (MAPK) in time- and concentration-dependent manners, and Rh2(S)-induced differentiation and mineralization of osteoblastic cells were totally inhibited in the presence of the p38 MAPK inhibitor, SB203580. In addition, pretreatment with Go6976, a protein kinase D (PKD) inhibitor, significantly reversed the Rh2(S)-induced p38 MAPK activation, indicating that PKD might be an upstream kinase for p38 MAPK in MC3T3-E1 cells. Taken together, these results suggest that Rh2(S) induces the differentiation and mineralization of MC3T3-E1 cells through activation of PKD/p38 MAPK signaling pathways, and these findings provide a molecular basis for the osteogenic effect of Rh2(S).

AMP-activated protein kinase: a potential target for ginsenosides?

Panax ginseng is a best-selling medicinal plant showing an antidiabetic activity via human, animal and in vitro studies. Among bioactive constituents found in ginseng, ginsenosides are known to be responsible for antidiabetic activity of ginseng. Ginsenoside Rb2, one of the major ginsenosides found in Asian ginseng, is shown to inhibit palmitate-induced gluconeogenesis in H4IIE rat hepatocytes via AMP-activated protein kinase (AMPK)-induced up-regulation of orphan nuclear receptor small heterodimer partner (SHP). Up to now, about thirteen articles were published to demonstrate that the pharmacological or physiological activities of ginsenosides are associated with AMPK, and only protopanaxatriol-type ginsenosides such as Re, Rg1 and Rg2, have been shown to suppress the hepatic glucose production. Therefore, Rb2 is the first protopanaxadiol-type ginsenoside shown to inhibit hepatic gluconeogenesis through AMPK activation. Further work will reveal whether activation of AMPK pathway by Rb2 would be beneficial to diabetic animals or type 2 diabetic patients.

Ginsenoside Rh2(S) induces differentiation and mineralization of MC3T3-E1 cells through activation of the PKD/AMPK signaling pathways.

As part of our search for biologically active anti-osteoporotic agents that enhance differentiation and mineralization of osteoblastic MC3T3-E1 cells, we identified the ginsenoside Rh2(S). Mostly known to exhibit beneficial effects in cancer prevention and metabolic diseases, Rh2(S) is one of the most active ginsenosides. Here, we show that Rh2(S) stimulates osteoblastic differentiation and mineralization, manifested by the up-regulation of differentiation markers (alkaline phosphatase and osteogenic genes) and von Kossa/Alizarin Red staining, respectively. Rh2(S) also activated protein kinase D (PKD) and AMP-activated protein kinase (AMPK) in a time- and concentration-dependent manner, and Rh2(S)-induced differentiation and mineralization of osteoblastic cells were significantly abolished in the presence of specific inhibitors; Go6976 for PKD and Ara-A for AMPK. Furthermore, Go6976 suppressed Rh2(S)-mediated activation of AMPK, indicating that PKD may be an upstream signal for AMPK in Rh2(S)-induced differentiation and mineralization of MC3T3-E1 cells. Taken together, these results indicate that Rh2(S) induces the differentiation and mineralization of MC3T3-E1 cells through activation of PKD/AMPK signaling pathways. These findings provide a molecular basis for the osteogenic effect of Rh2(S).

Anti-Diabetic Effect of Pectinase-Processed Ginseng Radix (GINST) in High Fat Diet-Fed ICR Mice.

In the present study, we investigate anti-diabetic effect of pectinase-processed ginseng radix (GINST) in high fat diet-fed ICR mice. The ICR mice were divided into three groups: regular diet group, high fat diet control group (HFD), and GINST-treated group. To induce hyperglycemia, mice were fed a high fat diet for 10 weeks, and mice were administered with 300 mg/ kg of GINST once a day for 5 weeks. Oral glucose tolerance test revealed that GINST improved glucose tolerance after glucose challenge. Compared to the HFD control group, fasting blood glucose and insulin levels were decreased by 57.8% (p<0.05) and 30.9% (p<0.01) in GINST-treated group, respectively. With decreased plasma glucose and insulin levels, the insulin resistance index of the GINST-treated group was reduced by 68.1% (p<0.01) compared to the HFD control group. Pancreas of GINST-treated mice preserved a morphological integrity of islets and consequently having more insulin contents. In addition, GINST up-regulated the levels of phosphorylated AMP-activated protein kinase (AMPK) and its target molecule, glucose transporter 4 (GLUT4) protein expression in the skeletal muscle. Our results suggest that GINST ameliorates a hyperglycemia through activation of AMPK/ GLUT4 signaling pathway, and has a therapeutic potential for type 2 diabetes.