Myeloperoxidase in chronic kidney disease: role of visceral fat.

AIM: Visceral fat is more significantly correlated with inflammation markers and oxidative stress than is subcutaneous fat. Myeloperoxidase is one inflammatory signal secreted after polymorphonuclear leukocytes are stimulated. However, few studies discuss the correlation between visceral fat and the inflammatory response in patients with chronic kidney disease (CKD). METHODS: Sixty-six patients with CKD were enrolled and 60 healthy participants. Visceral fat levels were obtained using bioelectrical impedance analysis. Traditional risk factors for myeloperoxidase were analyzed. RESULTS: Baseline myeloperoxidase levels were significantly different between patients and controls, and were correlated with visceral fat after they had been adjusted for residual renal function. A multivariate linear regression model revealed that the neutrophil count and visceral fat and serum albumin levels were significant predictors of plasma myeloperoxidase in patients with CKD, but not in controls. The neutrophil count was correlated with myeloperoxidase only in the CKD group. CONCLUSION: Visceral fat predicted plasma myeloperoxidase in patients with CKD, but not in healthy controls. Myeloperoxidase was probably contributed by primed and activated neutrophils that had been irritated by visceral fat in patients with CKD.

Short-term glutamine supplementation decreases lung inflammation and the receptor for advanced glycation end-products expression in direct acute lung injury in mice.

BACKGROUND: Glutamine (GLN) has been reported to improve clinical and experimental sepsis outcomes. However, the mechanisms underlying the actions of GLN remain unclear, and may depend upon the route of GLN administration and the model of acute lung injury (ALI) used. The aim of this study was to investigate whether short-term GLN supplementation had an ameliorative effect on the inflammation induced by direct acid and lipopolysaccharide (LPS) challenge in mice. METHODS: Female BALB/c mice were divided into two groups, a control group and a GLN group (4.17% GLN supplementation). After a 10-day feeding period, ALI was induced by intratracheal administration of hydrochloric acid (pH 1.0; 2 mL/kg of body weight [BW]) and LPS (5 mg/kg BW). Mice were sacrificed 3 h after ALI challenge. In this early phase of ALI, serum, lungs, and bronchoalveolar lavage fluid (BALF) from the mice were collected for further analysis. RESULTS: The results of this study showed that ALI-challenged mice had a significant increase in myeloperoxidase activity and expression of interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α in the lung compared with unchallenged mice. Compared with the control group, GLN pretreatment in ALI-challenged mice reduced the levels of receptor for advanced glycation end-products (RAGE) and IL-1ß production in BALF, with a corresponding decrease in their mRNA expression. The GLN group also had markedly lower in mRNA expression of cyclooxygenase-2 and NADPH oxidase-1. CONCLUSIONS: These results suggest that the benefit of dietary GLN may be partly contributed to an inhibitory effect on RAGE expression and pro-inflammatory cytokines production at an early stage in direct acid and LPS-induced ALI in mice.

trans-10,cis-12 conjugated linoleic acid specifically increases tissue α-tocopherol mediated by PPARγ inhibition in mice.

C57BL/6J mice were divided into control group (C), CLA, c9t11, or t10c12 groups. CLA and t10c12 significantly increased α-tocopherol levels in the plasma and various tissues in experiment 1. The CLA and t10c12 groups also showed a significant increase in hepatic α-tocopherol transfer protein (α-TTP) levels. In experiment 2, mice were divided into control, CLA, R (rosiglitazone, a PPARγ agonist), or CLA+R groups. Vitamin E levels in the liver, epididymal fat pad, kidney, and plasma were increased by CLA, and this effect was reduced in the CLA+R group. t10,c12-CLA is the most active isomer in the CLA mixture in the regulation of tissue vitamin E status and α-TTP protein levels in mice. The increase in liver vitamin E status in CLA-fed mice is mainly due to the effect of PPARγ inhibition.

Dietary oxidised frying oil causes oxidative damage of pancreatic islets and impairment of insulin secretion, effects associated with vitamin E deficiency.

We previously reported that, in rodents, a diet with a high oxidised frying oil (OFO) content leads to glucose intolerance associated with a reduction in insulin secretion. The present study aimed at investigating the impairment of pancreatic islets caused by dietary OFO. C57BL/6J mice were divided into three groups to receive a low-fat basal diet containing 5 g/100 g of fresh soyabean oil (LF group) or a high-fat diet containing 20 g/100 g of either fresh soyabean oil (HF group) or OFO (HO group). After 8 weeks, mice in the HO group showed glucose intolerance and hypoinsulinaemia, and their islets showed impaired glucose-stimulated insulin secretion (P < 0·05; HO group v. LF and HF groups). Significantly higher oxidative stress and a lower mitochondrial membrane potential were observed in the islets in the HO group compared with the LF and HF groups. Immunoblots showed that the reduction in insulin levels in HO islets was associated with activation of the c-Jun NH2-terminal kinase and a reduction in levels of pancreatic and duodenal homeobox factor-1. In a second study, when dietary OFO-induced tissue vitamin E depletion was prevented by large-dose vitamin E supplementation (500 IU(1·06 mmol all-rac-α-tocopherol acetate)/kg diet; HO+E group), the OFO-mediated reduction in islet size and impairment of glucose tolerance and insulin secretion were significantly attenuated (P < 0·05; HO group v. HO+E group). We conclude that a high level of dietary OFO ingestion impairs glucose metabolism by causing oxidative damage and compromising insulin secretion in pancreatic islets, and that these effects can be prevented by vitamin E supplementation.

Consuming oxidative frying oil impairs cardiac energy production and calcium recycling, causing cardiac hypertrophy, fibrosis and diastolic dysfunction in male Sprague Dawley rats.

With regards to cardiovascular health, frequent consumption of fried foods is discouraged, despite a lack of clear evidence of a direct link between eating oxidative frying oil (OFO) and cardiovascular diseases. In this study, male Sprague Dawley rats were exposed to diets containing fresh or fried soybean oil (groups C and O, respectively) from in utero to 28 weeks of age. A subset of rats in group O was supplemented with vitamin E (500 mg/kg of DL-α-tocopherol acetate; group OE) from 8 week of age onward to mitigate oxidative stress associated with OFO ingestion. Echocardiography, cardiac histology and indices associated with ATP production and calcium cycling in cardiac tissues were measured. Compared to group C, there was cardiac hypertrophy, fibrosis and diastolic dysfunction, in groups O and OE, with no differences between the latter two groups. Although cardiac mRNA levels of genes associated with mitochondrial biogenesis and function were increased, there were lower ATP concentrations and higher transcripts of uncoupling proteins in groups O and OE than in group C. In addition, decreases in phosphorylation of phospholamban and Ca2+/calmodulin-dependent protein kinase II activity, plus increased protein phosphatase 2A activity in groups O and OE, implied calcium cycling required for cardiac function was disrupted by OFO consumption. We concluded that long-term OFO exposure resulted in cardiac hypertrophy, fibrosis and diastolic dysfunction that was not mitigated by vitamin E supplementation. Underlying mechanisms were partly attributed to inefficient energy production via uncoupled phosphorylation and disrupted calcium cycling.

Liquid Chicken Oil Could Be a Healthy Dietary Oil.

Liquid chicken oil is similar to the human lipid ratio, and is similar to the ideal fatty acids ratio suggested by Hayes, but its benefits remain unclear (Hwang, K.N.; Tung, H.P.; Shaw, H.M. J. Oleo. Sci. 69, 199-206 (2020)). Using soybean oil as a control, liquid chicken oil, coconut oil, lard oil, and olive oil, were tested on SD rats with the rodent diet 5001 plus 1% of high cholesterol addition and moderate 10 % of test oils. Positive results showed that a 10% liquid chicken oil diet reduced LDL and triglycerides, atherogenic index while increasing superoxide dismutase more than the soybean oil control (0.05 ≦ p < 0.10). Moreover, increment of hepatic endogenous glutathione peroxidase was found to be significantly different from the soybean oil control (p < 0.05). In this study, liquid chicken oil had more benefits than vegetable soybean dietary oil, with little evidence of hyperlipidemia. Comparison of the test oils with categories of fatty acids to the idea ratio SFA : MUFA : PUFA = 1 : 1.5 : 1, scored by its average weight implied a parallel trend of lipidemia and hepatic antioxidant activity to its score. It is difficult to use the test of rat to reflect human physiology, it remain 19% different of the fatty acids ratio from human ratio, however, this study reveal that the healthiness of a dietary oil seems relate well to its compatibility to the idea ratio or the host oil ratio, in this case, it is the human ratio.

Adherence to Nutritional Supplementation Determines Postoperative Vitamin D Status, but Not Levels of Bone Resorption Marker, in Sleeve-Gastrectomy Patients.

BACKGROUND: Taking advantage of isomeric form of vitamin E in the supplement, adherence to supplement could be evaluated by changes in circulating α- and γ-tocopherol concentrations. Accordingly, effects of supplementation on postoperative nutrition and bone metabolism were studied in terms of adherence. METHODS: Thirty-eight SG patients were all prescribed a postoperative nutritional supplement containing a low dose of vitamin D (600 IU) and calcium (200 mg). Blood samples were collected prior to (M0) and 6 months after (M6) surgery and concentrations of nutrients and C-terminal telopeptide of type I collage (CTX), a marker of bone resorption, were measured. Adherence and non-adherence were stratified according to change (△, M6-M0) in serum α-tocopherol concentrations (> 0 vs. ≤ 0, respectively). RESULTS: When M0 and M6 were compared, there were significant increases in serum concentrations of 25(OH)D, α-tocopherol and selenium, whereas there were reductions in parathyroid hormone, ferritin, and γ-tocopherol. At M6, the prevalence of vitamin D insufficiency (25(OH)D < 30 ng/mL) and high CTX were 72 and 26%, respectively. When comparison was made between adherence and non-adherence, only △25(OH)D concentrations, but no other nutrients nor postoperative CTX differed. Multiple linear regression demonstrated that postoperative vitamin D status was independently associated with its preoperative concentrations (ß = 0.85, p < 0.001) and adherence (ß = 0.52, p < 0.05). CONCLUSION: SG patients' adherence to supplementation, even with a low dose of vitamin D and calcium, determined vitamin D status but not bone resorption marker concentrations, at least within 6 months after surgery.

Conjugated linoleic acid causes a marked increase in liver alpha-tocopherol and liver alpha-tocopherol transfer protein in C57BL/6 J mice.

Conjugated linoleic acid (CLA) is a collective term for the positional and geometric isomers of a conjugated diene of linoleic acid (C18:2, n-6). The aims of the present study were to evaluate whether levels of hepatic alpha-tocopherol, alpha-tocopherol transfer protein (alpha-TTP), and antioxidant enzymes in mice were affected by a CLA-supplemented diet. C57BL/6 J mice were divided into the CLA and control groups, which were fed, respectively, a 5 % fat diet with or without 1 g/100 g of CLA (1:1 mixture of cis-9, trans-11 and trans-10, cis-12) for four weeks. alpha-Tocopherol levels in plasma and liver were significantly higher in the CLA group than in the control group. Liver alpha-TTP levels were also significantly increased in the CLA group, the alpha-TTP/beta-actin ratio being 2.5-fold higher than that in control mice (p<0.01). Thiobarbituric acid-reactive substances were significantly decreased in the CLA group (p<0.01). There were no significant differences between the two groups in levels of three antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and catalase). The accumulation of liver alpha-tocopherol seen with the CLA diet can be attributed to the antioxidant potential of CLA and the ability of alpha-TTP induction. The lack of changes in antioxidant enzyme protein levels and the reduced lipid peroxidation in the liver of CLA mice are due to alpha-tocopherol accumulation.

Beyond the Recycle of Raw Chicken Fat.

The wasted raw fat of chicken was extracted and recrystallized with slowly stir at various cooling temperature to get a clear out-looking and liquid chicken oil. The recovery percentage of liquid chicken oil is about 100, 87, 78, 49 and 0% at 25, 21, 17, 13 and 9°C. The chicken liquid oil has a new composition of fatty acids than the original oil (p < 0.05) and has a safety range in acid value and peroxide value. The fatty acid ratio of the liquid chicken oil obtained at 13°C to be 1:1.6:0.9 (SFA: MUFA: PUFA) is believed to be good dietary oil. The concept of ideal fatty acid ratio comes from Hayes' report (1:1.5:1, SFA: MUFA: PUFA) which is also found to mimic to human lipid fatty acid ratio. Statistically evaluation on Hayes' basis, it showed that the liquid chicken oil scored even better than the extra virgin olive oil. In conclusion, this study not only first open a new gate for the recycle of global raw chicken fat to a dietary oil but also give an evidence that the chicken oil seems more compatible to human lipid on the hypothetic basis of biocompatibility.

Nutritional Status of Obese Taiwanese Before Bariatric-Metabolic Surgery and Their Serum 25-Hydroxyvitamin D Concentrations for Maximal Suppression of Parathyroid Hormone.

BACKGROUND: This is the first report from Taiwan using laboratory tests to assess nutritional status of patients with obesity before bariatric-metabolic surgery. Moreover, the 25(OH)D threshold for maximal suppression of parathyroid hormone (PTH) was evaluated to offer a reference value for preoperative nutritional care. METHODS: Inclusion criteria were Taiwanese, 18-65 years old, and with BMI ≥ 27.5 kg/m2 awaiting bariatric-metabolic surgery. Anthropometric data and blood samples were collected before surgery. Serum concentrations of protein; vitamins B1, B12, folate, A, D, and E; calcium; iron; zinc; copper; selenium; PTH; and erythrocyte glutathione reductase activity coefficient (vitamin B2 status) were measured. RESULTS: For 52 participants with a mean BMI 37.6 ± 6.4 kg/m2, vitamin D deficiency (25(OH)D < 20 ng/mL) and insufficiency (20 < 25(OH)D < 30 ng/mL) were at 73 and 22% prevalence, respectively. Secondary hyperparathyroidism (PTH â‰§ 65 pg/mL) was 24% and hypocalcemia was 50% (ionized Ca < 4.5 mg/dL). Deficiency of other nutrients was sporadic (< 10%) or nil. When participants were stratified according to 25(OH)D concentrations (< 10, 10-15, 15-20, and ≥ 20 ng/mL), PTH increased at 25(OH)D < 10 ng/mL (ß = 48.34, p = 0.001) after adjusting for age, gender, and BMI. CONCLUSION: For patients with obesity before bariatric-metabolic surgery, vitamin D/calcium deficiency was the only nutritional issue that needs to be addressed in Taiwan. However, a lower cutoff point of 25(OH)D, i.e., 10 ng/mL, for vitamin D deficiency may be considered for patients before surgery. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03915158.

Effects of Oxidized Frying Oil on Proteins Related to alpha-Tocopherol Metabolism in Rat Liver.

An oxidized frying oil (OFO) diet has been reported to induce an increase in lipid peroxidation and a reduction in vitamin E status in animal tissues. This study was performed to investigate how vitamin E metabolism is influenced by OFO. Male Wistar rats were divided into three groups, a control group (CO) and two OFO-fed groups (OF and OFE). The diet of the OFE group was supplemented with an extra 50 mg/kg of alpha-tocopherol acetate and thus contained twice as much vitamin E as that of the OF group. After six weeks on these diets, liver alpha-tocopherol levels in the OF group were the significantly lowest among the three groups. Excretion of the alpha-tocopherol metabolite, alpha-carboxyethyl hydroxychroman (alpha-CEHC) in the urine was significantly lower in the OF group than in the other two groups. There were no significant differences in protein levels of alpha-tocopherol transfer protein (alpha-TTP) and multidrug resistance protein among the three groups. Protein levels of cytochrome P450 monooxygenase (CYP) 3A, CYP4A, and catalase were markedly increased in both groups on the OFO diet. This suggests that an OFO diet may interfere with medicine metabolism and needs further investigation.

Impairment of glucose metabolism in mice induced by dietary oxidized frying oil is different from that induced by conjugated linoleic acid.

OBJECTIVE: We previously reported that a diet high in oxidized frying oil (OFO) is less adipogenic but induces glucose intolerance in rodents, a situation somewhat is similar to that in conjugated linoleic acid (CLA)-fed mice. The present study compared the lipid and glucose metabolism effects of dietary OFO and CLA to clarify how the OFO diet compromises glucose tolerance. METHODS: C57BL/6J mice were divided into four groups in which the CLA and CLA control (CC) groups received a low-fat diet supplemented with or without 1 g/100 g of CLA (1:1 mixture of cis-9, trans-11 and trans-10, cis-12), and the OFO and OFO control (CO) groups received a high-fat diet containing 20 g/100 g of OFO or fresh soybean oil, respectively. RESULTS: When compared with their respective controls (CLA versus CC and OFO versus CO), the OFO and CLA diets resulted in deprivation of adipose and downregulation of adipocyte marker genes, but a totally different response of lipid metabolism in the liver was observed, i.e., anabolism was enhanced by the CLA diet but catabolism was enhanced by the OFO diet. In contrast to the insulin resistance that occurred in CLA-fed mice, the glucose intolerance induced by the OFO diet was accompanied by decreases in insulin and C-peptide levels during an oral glucose tolerance test. Analysis of vitamin E and thiobarbituric acid-reactive substances in the liver showed the OFO diet, but not the CLA diet, compromised vitamin E status. CONCLUSION: The impaired glucose metabolism resulting from OFO feeding is not related to CLA. In contrast to the hyperinsulinemia and insulin resistance induced by the CLA diet, the OFO diet-induced glucose intolerance is mediated by impairment of insulin secretion.

Pregnenolone and dexamethasone, modulators of cytochrome P450-3A, not increase but reduce urinary alpha-CEHC excretion in rats.

In this study, the CYP3A inducer pregnenolone-16alpha-carbonitrile (PCN) and the CYP3A inhibitor ketoconazole (KCZ) were used to investigate whether the metabolism of alpha-tocopherol to its metabolite, alpha-carboxyethyl hydroxychroman (alpha-CEHC), is CYP3A-dependent in rats. In experiment 1, two groups of Wistar rats were fed for 3 wk with either a basal diet (containing 50 ppm of alpha-tocopherol) or the same diet containing 10-fold more alpha-tocopherol. In the last 3 days, each group was divided into 2 subgroups which were given a single i.p. injection of either PCN at 75 mg/kg/d (P50 & P500 groups) or DMSO (D50 & D500 groups). The liver TBARS concentration was highest in the P50 group. Two-way ANOVA analysis showed that alpha-tocopherol levels in the plasma and liver were both significantly decreased by PCN (p < 0.0001), as were alpha-CEHC levels in the urine (p = 0.0004). In experiment 2, alpha-tocopherol levels in the liver were increased and alpha-CEHC excretion in the urine decreased in the Wistar rats fed with KCZ containing diet. In experiment 3, Wistar rats administered with dexamethasone (DEX) significantly decreased alpha-tocopherol levels in the plasma and liver and alpha-CEHC levels in the urine. These data showed CYP3A is not a major contributor of the metabolism of alpha-tocopherol to alpha-CEHC. Nevertheless, vitamin E status was markedly reduced by CYP3A inducers due to increased lipid peroxidation and this would increase the consumption of alpha-tocopherol in the liver.

Elevation of tissue α-tocopherol levels by conjugated linoleic acid in C57BL/6J mice is not associated with changes in vitamin E absorption or α-carboxyethyl hydroxychroman production.

OBJECTIVE: Conjugated linoleic acid (CLA) decreases adipose mass and increases vitamin E levels in the liver and adipose tissue in mice. The aim of the present study was to examine the mechanism by which CLA alters vitamin E levels in tissues and antioxidant activity in mice. METHODS: C57BL/6J mice were divided into three groups and fed 5% lipid as soybean oil alone (control group), 4% soybean oil supplemented with 1% CLA (CLA group), or 5% lipid with a vitamin E supplement (VE group) for 4 wk. RESULTS: The CLA and VE diets resulted in a significant increase in the α-tocopherol concentration in all tissues examined, i.e., the liver, kidney, testis, spleen, heart, lung, and adipose tissue (P < 0.05). Levels of thiobarbituric acid-reactive substances in the kidney, testis, heart, lung, and adipose tissue were lower in the CLA and VE groups than in the control group (P < 0.05). CLA did not alter the absorption rate of vitamin E or α-carboxyethyl hydroxychromans levels in the liver and plasma. The CLA diet induced a significant increase in α-tocopherol transfer protein and mRNA levels in the liver. CLA resulted in a decrease in catalase and glutathione peroxidase activities and peroxisome proliferator α mRNA levels but had no effect on levels of mRNAs for other nuclear transcription factors in the liver. CONCLUSION: The increase in vitamin E status in CLA-fed mice is not due to altered absorption and metabolism of vitamin E but might be related to the induction of α-tocopherol transfer protein expression in the liver. The regulation of the activities of catalase and glutathione peroxidase by CLA is not mediated by vitamin E accumulation in the liver.

Effects of pregnenolone-16alpha-carbonitrile on vitamin E status and protein levels of antioxidant enzymes in male rats fed a vitamin E-supplemented diet.

The aim of this study was to evaluate the effects of the administration of pregnenolone-16alpha-carbonitrile (PCN), an inducer of the cytochrome P450 3A gene in rats, on vitamin E status and antioxidant enzyme protein levels in rats fed a vitamin E-supplemented diet. Two groups of male Wistar rats were fed for 3 weeks with a basal diet containing 50 ppm of alpha-tocopherol or the same diet containing 10 times more alpha-tocopherol. In the final 3 days, each group was divided into two subgroups which were given a single daily intraperitoneal injection of PCN at 75 mg/kg (groups PCN and PCN+VE) or DMSO (groups DS and DS+VE). PCN treatment alone significantly reduced the alpha-tocopherol content of the liver and plasma and this effect was prevented by supplementation with 10-fold more alpha-tocopherol. alpha-Tocopherol levels in the kidneys, lung, heart, and testes were significantly higher in both vitamin E-supplemented groups than in the control groups. TBARS levels in the liver and lung were significantly increased in both PCN-treated groups, as shown by two-way ANOVA analysis. PCN also caused a significant reduction in protein levels of catalase and glutathione peroxidase (GPx) in both groups. Dietary vitamin E supplementation caused a decrease in liver protein levels of GPx and superoxide dismutase, but not catalase, in both groups and protected against PCN-induced lipid peroxidation, which was caused by CYP3A induction and a reduction in antioxidant enzyme levels.