Hypopurolides A - G, Labdane Diterpenoids from Hypoestes purpurea and Their Nitric Oxide Inhibitory Activity.

Seven new labdane diterpenoids, hypopurolides A-G (1-7) were discovered from the aerial part of Hypoestes purpurea, along with one known analog, hypopurin D (8). The structures of 1-7 were characterized based on 1 H-, 13 C-, and 2D-NMR, and HR-ESI-MS spectra. The absolute configurations of 1-7 were defined by single-crystal X-ray diffraction and electronic circular dichroism (ECD) data. Compounds 1-8 were tested for their nitric oxide (NO) inhibitory and cytotoxic effects. Compound 6 displayed moderate inhibitory effect toward LPS-induced NO release in RAW 264.7 cells with an IC50 value of 41.50 µM.

Four Highly Oxygenated Sesquiterpenoids from the Fruits of Illicium micranthum Dunn.

Four highly oxygenated sesquiterpenoids, illimicranolides A (1) and B (2), and illicinolides E (3) and F (4), were obtained from the fruits of Illicium micranthum Dunn, as well as one known analog, illicinolide B (5). The chemical structures of 1-4 were determined comprehensively by 1D (1 H and 13 C) and 2D (HMBC, HSQC, 1 H-1 H COSY, and ROESY) NMR, and HR-ESI-MS data. Structurally, compound 1 was an unprecedented sesquiterpenoid with a 5/5/6/5-fused tetracyclic ring system and was the first seco-prezizaane sesquiterpenoid featuring a 11,8-γ-lactone ring. Compounds 3 and 4 were the fifth and sixth examples of illicinolide-type sesquiterpenoids. Moreover, compound 1 demonstrated neurotrophic activity of NGF-induced PC12 cells with differentiation rate of 10.34 % at a concentration of 10 µM.

[16-gauge vs 18-gauge puncture needle for transrectal ultrasound-guided prostate biopsy in the diagnosis of prostate cancer: Effect and complications].

OBJECTIVE: To compare the efficiency and complications of transrectal ultrasound (TRUS)-guided prostate biopsy with a 16-gauge (16G) or an 18G puncture needle in the diagnosis of PCa. METHODS: This prospective randomized controlled study included 142 male patients undergoing TRUS-guided prostate biopsy in our hospital, 71 with the 16G and the other 71 with the 18G puncture needle. We compared the post-puncture incidence rates of hematuria, bleeding and infection between the two groups of patients and classified the complications according to the Clavien-Dindo scores. RESULTS: The detection rate of PCa was significantly lower in the 18G than in the 16G group (12.68% vs 36.62%, χ2 = 10.958, P = 0.001), even with f/tPSA ≤ 0.15 (8.51% vs 44.44%, χ2 = 12.617, P = 0.001), but showed no statistically significant difference between the two groups with f/tPSA > 0.15 (P<0.05). No post-puncture infection was observed in any of the patients. There were no statistically significant differences between the 18G and 16G groups in the incidence rates of rectal bleeding (21.13% vs 15.49%, χ2 = 0.753, P = 0.385) and urethral bleeding (18.31% vs 16.90%, χ2 = 0.049, P = 0.826), nor in Clavien-Dindo grades (26 vs 20 cases of grade I; no grade II in either group; 2 vs 3 cases of grade III ; Z = －0.698, P = 0.458). CONCLUSIONS: The 16G puncture needle can achieve a higher detection rate of PCa than the 18G needle in TRUS-guided prostate biopsy without increasing the incidence of complications.

Effects of dietary addition of heat-killed Mycobacterium phlei on growth performance, immune status and anti-oxidative capacity in early weaned piglets.

The contradiction between high susceptibility of early weaned piglets to enteric pathogens and rigid restriction of antibiotic use in the diet is still prominent in the livestock production industry. To address this issue, the study was designed to replace dietary antibiotics partly or completely by an immunostimulant, namely heat-killed Mycobacterium phlei (M. phlei). Piglets (n = 192) were randomly assigned to one of the four groups: (1) basal diet (Group A), (2) basal diet + a mixture of antibiotics (80 mg/kg diet, Group B), (3) basal diet + a mixture of antibiotics (same as in Group B, but 40 mg/kg diet) + heat-killed M. phlei (1.5 g/kg diet) (Group C) and (4) basal diet + heat-killed M. phlei (3 g/kg diet) (Group D). All piglets received the respective diets from days 21 to 51 of age and were weaned at the age of 28 d. Compared with the Control (Group A), in all other groups the average daily gain, average daily feed intake, small intestinal villus height:crypt depth ratio and protein levels of occludin and ZO-1 in the jejunal mucosa were increased. A decreased incidence of diarrhoea in conjunction with an increased sIgA concentration in the intestinal mucosa and serum IL-12 and IFN-γ concentrations was found in groups supplemented with heat-killed M. phlei (Groups C and D), but not in Group B. Groups C and D also showed decreased IL-2 concentrations in the intestinal mucosa with lower TLR4 and phosphor-IκB protein levels. The antioxidant capacity was reinforced in Groups C and D, as evidenced by the reduction in malondialdehyde and enhanced activities of antioxidant enzymes in serum. These data indicate that heat-killed M. phlei is a promising alternative to antibiotic use for early weaned piglets via induction of protective immune responses.

[Expressions of Cx26, Cx32 and Cx43 in prostate cancer and their implications].

OBJECTIVE: To investigate the expressions of Cx26, Cx32 and Cx43 in prostate cancer (PCa) and benign prostatic hyperplasia (BPH) and their roles in the development and progression of PCa in order to provide some novel evidence for the diagnosis and treatment of PCa. METHODS: We determined the expressions of Cx26, Cx32 and Cx43 in the paraffin samples from 31 cases of PCa and 23 cases of BPH by SABC immunohistochemical staining, and analyzed the relationship of their expressions with the clinical and pathological parameters of PCa and BPH using the semiquantitative method. RESULTS: The positive expressions of Cx26 in BPH and PCa were 82.6% and 74.2%, respectively (chi2 = 0.541, P > 0.05), those of Cx32 were 78.3% and 61.3% (chi2 = 1.763, P > 0.05), and those of Cx43 were 87.0% and 38.7% (chi2 = 12.730, P < 0.01). The staining intensities of Cx26 and Cx43 were negatively correlated with the malignant phenotype of PCa (rCx26 = -0.476, P < 0.01; rCx43 = -0.484, P < 0.01), but not the expression of Cx32 (r = -0.242, P > 0.05). The three Cxs exhibited no correlation with the age and serum PSA level of the patients (P > 0.05), nor among their expressions (P > 0.05). CONCLUSION: Cx26, Cx32 and Cx43 are expressed in different degrees in BPH and PCa tissues. Cx43 plays a role in the occurrence and progression of PCa, and may serve as a new marker of PCa besides PSA as well as a new target in the biotherapy of PCa. Cx26 may be partially involved in the progression of PCa, but its mechanisms need to be further studied.

Aging-associated reductions in AMP-activated protein kinase activity and mitochondrial biogenesis.

Recent studies have demonstrated a strong relationship between aging-associated reductions in mitochondrial function, dysregulated intracellular lipid metabolism, and insulin resistance. Given the important role of the AMP-activated protein kinase (AMPK) in the regulation of fat oxidation and mitochondrial biogenesis, we examined AMPK activity in young and old rats and found that acute stimulation of AMPK-alpha(2) activity by 5'-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and exercise was blunted in skeletal muscle of old rats. Furthermore, mitochondrial biogenesis in response to chronic activation of AMPK with beta-guanidinopropionic acid (beta-GPA) feeding was also diminished in old rats. These results suggest that aging-associated reductions in AMPK activity may be an important contributing factor in the reduced mitochondrial function and dysregulated intracellular lipid metabolism associated with aging.

Paradoxical effects of increased expression of PGC-1alpha on muscle mitochondrial function and insulin-stimulated muscle glucose metabolism.

Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha has been shown to play critical roles in regulating mitochondria biogenesis, respiration, and muscle oxidative phenotype. Furthermore, reductions in the expression of PGC-1alpha in muscle have been implicated in the pathogenesis of type 2 diabetes. To determine the effect of increased muscle-specific PGC-1alpha expression on muscle mitochondrial function and glucose and lipid metabolism in vivo, we examined body composition, energy balance, and liver and muscle insulin sensitivity by hyperinsulinemic-euglycemic clamp studies and muscle energetics by using (31)P magnetic resonance spectroscopy in transgenic mice. Increased expression of PGC-1alpha in muscle resulted in a 2.4-fold increase in mitochondrial density, which was associated with an approximately 60% increase in the unidirectional rate of ATP synthesis. Surprisingly, there was no effect of increased muscle PGC-1alpha expression on whole-body energy expenditure, and PGC-1alpha transgenic mice were more prone to fat-induced insulin resistance because of decreased insulin-stimulated muscle glucose uptake. The reduced insulin-stimulated muscle glucose uptake could most likely be attributed to a relative increase in fatty acid delivery/triglyceride reesterfication, as reflected by increased expression of CD36, acyl-CoA:diacylglycerol acyltransferase1, and mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase, that may have exceeded mitochondrial fatty acid oxidation, resulting in increased intracellular lipid accumulation and an increase in the membrane to cytosol diacylglycerol content. This, in turn, caused activation of PKC, decreased insulin signaling at the level of insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, and skeletal muscle insulin resistance.

Prevention of hepatic steatosis and hepatic insulin resistance in mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 knockout mice.

In order to investigate the role of mitochondrial acyl-CoA:glycerol-sn-3-phosphate acyltransferase 1 (mtGPAT1) in the pathogenesis of hepatic steatosis and hepatic insulin resistance, we examined whole-body insulin action in awake mtGPAT1 knockout (mtGPAT1(-/-)) and wild-type (wt) mice after regular control diet or three weeks of high-fat feeding. In contrast to high-fat-fed wt mice, mtGPAT1(-/-) mice displayed markedly lower hepatic triacylglycerol and diacylglycerol concentrations and were protected from hepatic insulin resistance possibly due to a lower diacylglycerol-mediated PKC activation. Hepatic acyl-CoA has previously been implicated in the pathogenesis of insulin resistance. Surprisingly, compared to wt mice, mtGPAT1(-/-) mice exhibited increased hepatic insulin sensitivity despite an almost 2-fold elevation in hepatic acyl-CoA content. These data suggest that mtGPAT1 might serve as a novel target for treatment of hepatic steatosis and hepatic insulin resistance and that long chain acyl-CoA's do not mediate fat-induced hepatic insulin resistance in this model.

Inhibition of protein kinase Cepsilon prevents hepatic insulin resistance in nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease is strongly associated with hepatic insulin resistance and type 2 diabetes mellitus, but the molecular signals linking hepatic fat accumulation to hepatic insulin resistance are unknown. Three days of high-fat feeding in rats results specifically in hepatic steatosis and hepatic insulin resistance. In this setting, PKCepsilon, but not other isoforms of PKC, is activated. To determine whether PKCepsilon plays a causal role in the pathogenesis of hepatic insulin resistance, we treated rats with an antisense oligonucleotide against PKCepsilon and subjected them to 3 days of high-fat feeding. Knocking down PKCepsilon expression protects rats from fat-induced hepatic insulin resistance and reverses fat-induced defects in hepatic insulin signaling. Furthermore, we show that PKCepsilon associates with the insulin receptor in vivo and impairs insulin receptor kinase activity both in vivo and in vitro. These data support the hypothesis that PKCepsilon plays a critical role in mediating fat-induced hepatic insulin resistance and represents a novel therapeutic target for type 2 diabetes.

Overexpression of uncoupling protein 3 in skeletal muscle protects against fat-induced insulin resistance.

Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and is strongly associated with obesity. Increased concentrations of intracellular fatty acid metabolites have been postulated to interfere with insulin signaling by activation of a serine kinase cascade involving PKCtheta in skeletal muscle. Uncoupling protein 3 (UCP3) has been postulated to dissipate the mitochondrial proton gradient and cause metabolic inefficiency. We therefore hypothesized that overexpression of UCP3 in skeletal muscle might protect against fat-induced insulin resistance in muscle by conversion of intramyocellular fat into thermal energy. Wild-type mice fed a high-fat diet were markedly insulin resistant, a result of defects in insulin-stimulated glucose uptake in skeletal muscle and hepatic insulin resistance. Insulin resistance in these tissues was associated with reduced insulin-stimulated insulin receptor substrate 1- (IRS-1-) and IRS-2-associated PI3K activity in muscle and liver, respectively. In contrast, UCP3-overexpressing mice were completely protected against fat-induced defects in insulin signaling and action in these tissues. Furthermore, these changes were associated with a lower membrane-to-cytosolic ratio of diacylglycerol and reduced PKCtheta activity in whole-body fat-matched UCP3 transgenic mice. These results suggest that increasing mitochondrial uncoupling in skeletal muscle may be an excellent therapeutic target for type 2 diabetes mellitus.

Reversal of diet-induced hepatic steatosis and hepatic insulin resistance by antisense oligonucleotide inhibitors of acetyl-CoA carboxylases 1 and 2.

Hepatic steatosis is a core feature of the metabolic syndrome and type 2 diabetes and leads to hepatic insulin resistance. Malonyl-CoA, generated by acetyl-CoA carboxylases 1 and 2 (Acc1 and Acc2), is a key regulator of both mitochondrial fatty acid oxidation and fat synthesis. We used a diet-induced rat model of nonalcoholic fatty liver disease (NAFLD) and hepatic insulin resistance to explore the impact of suppressing Acc1, Acc2, or both Acc1 and Acc2 on hepatic lipid levels and insulin sensitivity. While suppression of Acc1 or Acc2 expression with antisense oligonucleotides (ASOs) increased fat oxidation in rat hepatocytes, suppression of both enzymes with a single ASO was significantly more effective in promoting fat oxidation. Suppression of Acc1 also inhibited lipogenesis whereas Acc2 reduction had no effect on lipogenesis. In rats with NAFLD, suppression of both enzymes with a single ASO was required to significantly reduce hepatic malonyl-CoA levels in vivo, lower hepatic lipids (long-chain acyl-CoAs, diacylglycerol, and triglycerides), and improve hepatic insulin sensitivity. Plasma ketones were significantly elevated compared with controls in the fed state but not in the fasting state, indicating that lowering Acc1 and -2 expression increases hepatic fat oxidation specifically in the fed state. These studies suggest that pharmacological inhibition of Acc1 and -2 may be a novel approach in the treatment of NAFLD and hepatic insulin resistance.

Aqua-bis(2,2'-bipyridine-κN,N')(1H-indole-2-carboxyl-ato-κO)nickel(II) 1H-indole-2-carboxyl-ate dihydrate.

The hydro-thermal reaction of Ni(2)(OH)(2)CO(3) with 2,2'-bipyridine and 2-indolyl-formic acid in CH(3)OH/H(2)O at 423 K for 7 d produced the novel Ni(II) complex [Ni(C(9)H(6)NO(2))(C(10)H(8)N(2))(2)(H(2)O)](C(9)H(6)NO(2))·2H(2)O. The asymmetric unit of the title compound consists of a monovalent [Ni(L)(bpy)(2)(H(2)O)](+) cation (bpy is 2,2'-bipyridine and L is 1H-indole-2-carboxyl-ate), an L anion and two solvent water mol-ecules. In the [Ni(L)(bpy)(2)(H(2)O)](+) cations, the Ni atom coordinates to four N atoms from the two bpy ligands and two O atoms, one from a L anion and the other from a water mol-ecule to complete an significantly distorted NiN(4)O(2) octa-hedron. The coordinated and solvate water mol-ecules form an extensive series of O-H⋯O hydrogen bonds. N-H⋯O and C-H⋯O hydrogen bonds are also present and the mol-ecules are inter-linked, forming a three-dimensional network.

The polycystin-1 C-terminal fragment triggers branching morphogenesis and migration of tubular kidney epithelial cells.

Mutations of either PKD1 or PKD2 cause autosomal dominant polycystic kidney disease, a syndrome characterized by extensive formation of renal cysts and progressive renal failure. Homozygous deletion of Pkd1 or Pkd2, the genes encoding polycystin-1 and polycystin-2, disrupt normal renal tubular differentiation in mice but do not affect the early steps of renal development. Here, we show that expression of the C-terminal 112 amino acids of human polycystin-1 triggers branching morphogenesis and migration of inner medullary collecting duct (IMCD) cells, and support in vitro tubule formation. The integrity of the polycystin-2-binding region is necessary but not sufficient to induce branching of IMCD cells. The C-terminal domain of polycystin-1 stimulated protein kinase C-alpha (PKC-alpha), but not the extracellular signal-regulated kinases ERK1 or ERK2. Accordingly, inhibition of PKC, but not ERK, prevented polycystin-1-mediated IMCD cell morphogenesis. In contrast, HGF-mediated morphogenesis required ERK activation but was not dependent on PKC. Our findings demonstrate that the C-terminal domain of polycystin-1, acting in a ligand-independent fashion, triggers unique signaling pathways for morphogenesis, and likely plays a central role in polycystin-1 function.

PKC-theta knockout mice are protected from fat-induced insulin resistance.

Insulin resistance plays a primary role in the development of type 2 diabetes and may be related to alterations in fat metabolism. Recent studies have suggested that local accumulation of fat metabolites inside skeletal muscle may activate a serine kinase cascade involving protein kinase C-theta (PKC-theta), leading to defects in insulin signaling and glucose transport in skeletal muscle. To test this hypothesis, we examined whether mice with inactivation of PKC-theta are protected from fat-induced insulin resistance in skeletal muscle. Skeletal muscle and hepatic insulin action as assessed during hyperinsulinemic-euglycemic clamps did not differ between WT and PKC-theta KO mice following saline infusion. A 5-hour lipid infusion decreased insulin-stimulated skeletal muscle glucose uptake in the WT mice that was associated with 40-50% decreases in insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated PI3K activity. In contrast, PKC-theta inactivation prevented fat-induced defects in insulin signaling and glucose transport in skeletal muscle. In conclusion, our findings demonstrate that PKC-theta is a crucial component mediating fat-induced insulin resistance in skeletal muscle and suggest that PKC-theta is a potential therapeutic target for the treatment of type 2 diabetes.

Inactivation of fatty acid transport protein 1 prevents fat-induced insulin resistance in skeletal muscle.

Insulin resistance in skeletal muscle plays a major role in the development of type 2 diabetes and may be causally associated with increases in intramuscular fatty acid metabolites. Fatty acid transport protein 1 (FATP1) is an acyl-CoA synthetase highly expressed in skeletal muscle and modulates fatty acid uptake and metabolism by converting fatty acids into fatty acyl-CoA. To investigate the role of FATP1 in glucose homeostasis and in the pathogenesis of insulin resistance, we examined the effect of acute lipid infusion or chronic high-fat feeding on insulin action in FATP1 KO mice. Whole-body adiposity, adipose tissue expression of adiponectin, intramuscular fatty acid metabolites, and insulin sensitivity were not altered in FATP1 KO mice fed a regular chow diet. In contrast, FATP1 deletion protected the KO mice from fat-induced insulin resistance and intramuscular accumulation of fatty acyl-CoA without alteration in whole-body adiposity. These findings demonstrate an important role of intramuscular fatty acid metabolites in causing insulin resistance and suggest that FATP1 may be a novel therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Adipocyte-specific overexpression of FOXC2 prevents diet-induced increases in intramuscular fatty acyl CoA and insulin resistance.

Insulin resistance plays a major role in the development of type 2 diabetes and may be causally associated with increased intracellular fat content. Transgenic mice with adipocyte-specific overexpression of FOXC2 (forkhead transcription factor) have been generated and shown to be protected against diet-induced obesity and glucose intolerance. To understand the underlying mechanism, we examined the effects of chronic high-fat feeding on tissue-specific insulin action and glucose metabolism in the FOXC2 transgenic (Tg) mice. Whole-body fat mass were significantly reduced in the FOXC2 Tg mice fed normal diet or high-fat diet compared with the wild-type mice. Diet-induced insulin resistance in skeletal muscle of the wild-type mice was associated with defects in insulin signaling and significant increases in intramuscular fatty acyl CoA levels. In contrast, FOXC2 Tg mice were completely protected from diet-induced insulin resistance and intramuscular accumulation of fatty acyl CoA. High-fat feeding also blunted insulin-mediated suppression of hepatic glucose production in the wild-type mice, whereas FOXC2 Tg mice were protected from diet-induced hepatic insulin resistance. These findings demonstrate an important role of adipocyte-expressed FOXC2 on whole-body glucose metabolism and further suggest FOXC2 as a novel therapeutic target for the treatment of insulin resistance and type 2 diabetes.

Salidroside reduces renal cell carcinoma proliferation by inhibiting JAK2/STAT3 signaling.

Salidroside has been reported to exhibit anticancer properties. This study aimed to investigate the effects of salidroside on renal cell carcinoma growth. Cell viability and proliferation was assessed by Cell Counting Kit-8 and colony formation assays in A498 and 786-0 cells. The effects of salidroside on in vivo tumor growth were also assessed in a mouse xenograft model of renal cell carcinoma. Flow cytometry was used to analyze cell cycle and apoptosis and protein levels were determined by western blotting. Salidroside reduced cell viability and colony formation in both cell lines in a concentration- and time-dependent manner. Tumor growth was also suppressed in the mouse model. Furthermore, salidroside induced significant G1 phase cell cycle arrest and induced apoptosis in both A498 and 786-0 cells. Higher concentrations of salidroside reduced the levels of phosphorylated signal transducer and activator of transcription 3 (STAT3) and Janus kinase 2 (JAK2). These results suggested that salidroside produced potent anticancer properties in renal cell carcinoma by modulating JAK2/STAT3 signaling. Administration of salidroside to patients with renal cell carcinoma might provide a promising therapeutic strategy for this malignancy.

[Effects of irrigation and fertilization on soil microbial properties in summer maize field].

In order to investigate the effects of different irrigation and fertilization on soil microbial properties of summer maize field, we used ZN99 with high nitrogen use efficiency as the test material. The experiment adopted the split plot design which included two irrigation levels (526 mm and 263 mm) as the main plots, three fertilizer types (U, M, UM) and two fertilizer levels (N 100 kg . hm-2 and 200 kg . hm-2) as the subplots. The results showed that the irrigation level affected the regulating effects of fertilizer on soil microbial biomass (carbon and nitrogen) and microbial di- versity. The organic fertilizer application must be under the sufficient irrigation level to increase the soil MBC (14.3%-33.6%), MBN (1.8-2.3 times) and abundance significantly. A moderate rate of irrigation, higher rates of organic fertilizer application or organic manure combined with inorganic fertilizer could increase the nitrogen-fixation species and quantity of Firmicutes, γ-Proteobacteria and α-Proteobacteria in the soil. Under the same N level, there was no significant difference of grain yield between organic manure and inorganic fertilizer treatments. Considering sustainable production, proper organic manure application with moderate irrigation could increase the quantity of the soil microbial biomass and microbial diversity, and improve the capacity of soil to supply water and nutrients.

Arterially transplanted mesenchymal stem cells in a mouse reversible unilateral ureteral obstruction model: in vivo bioluminescence imaging and effects on renal fibrosis.

BACKGROUND: Chronic kidney disease (CDK) is a worldwide health problem, but there is currently no effective treatment that can completely cure this disease. Recently, studies with mesenchymal stem cells (MSCs) on treating various renal diseases have shown breakthroughs. This study is to observe the homing features of MSCs transplanted via kidney artery and effects on renal fibrosis in a reversible unilateral ureteral obstruction (R-UUO) model. METHODS: Thirty-six Balb/c mice were divided into UUO group, UUO-MSC group, and sham group randomly, with 12 mice in each group. The MSCs had been infected by a lentiviral vector to express stably the luciferase reporter gene and green fluorescence protein genes (Luc-GFP-MSC). Homing of MSCs was tracked using in vivo imaging system (IVIS) 1, 3, 14, and 28 days after transplantation. Imaging results were verified by detecting GFP expression in frozen section under a fluorescence microscope. E-cadherin, α-SMA, TGF-ß1, and TNF-α mRNA expression in all groups at 1 and 4 weeks after transplantation were analyzed by quantitative PCR. RESULTS: Transplanted Luc-GFP-MSCs showed increased Luciferase expression 3 days after transplantation. The expression decreased from 7 days, weakened thereafter and could not be detected 14 days after transplantation. Quantitative PCR results showed that all gene expressions in UUO group and UUO-MSC group at 1 week had no statistical difference, while at 4 weeks, except TGF-ß expression (P > 0.05), the expression of E-cadherin, α-SMA, and TNF-α in the above two groups have statistical difference (P < 0.01). CONCLUSION: IVIS enables fast, noninvasive, and intuitive tracking of MSC homing in vivo. MSCs can be taken home to kidney tissues of the diseased side in R-UUO model, and renal interstitial fibrosis can be improved as well.

Resistance to high-fat diet-induced obesity and insulin resistance in mice with very long-chain acyl-CoA dehydrogenase deficiency.

Mitochondrial fatty acid oxidation provides an important energy source for cellular metabolism, and decreased mitochondrial fatty acid oxidation has been implicated in the pathogenesis of type 2 diabetes. Paradoxically, mice with an inherited deficiency of the mitochondrial fatty acid oxidation enzyme, very long-chain acyl-CoA dehydrogenase (VLCAD), were protected from high-fat diet-induced obesity and liver and muscle insulin resistance. This was associated with reduced intracellular diacylglycerol content and decreased activity of liver protein kinase Cvarepsilon and muscle protein kinase Ctheta. The increased insulin sensitivity in the VLCAD(-/-) mice were protected from diet-induced obesity and insulin resistance due to chronic activation of AMPK and PPARalpha, resulting in increased fatty acid oxidation and decreased intramyocellular and hepatocellular diacylglycerol content.