Journal of nutrition & intermediary metabolism最新文献

Background

Studies have consistently shown that risk of type 2 diabetes (T2D) is positively associated with dietary haem iron intake and inversely associated with dietary magnesium intake in a dose-response way. However, interaction effects of these two clinically important nutrients on T2DM risk in a prospective setting is unknown.

Objective

To determine the five-year risk of developing impaired fasting glucose (IFG) associated with dietary magnesium-to-iron intake ratios (Mg/Fe), including Mg/total Fe, Mg/haem-Fe and Mg/non-haem Fe.

Design

A cohort study of 1056 participants recruited into the Jiangsu Nutrition Study (JIN) from 2002 to 2007, aged at least 20 years and without known diabetes and IFG at baseline were followed up for five years. Dietary magnesium and iron intake at baseline was assessed by 3-day weighed food records. Fasting plasma glucose was measured both at baseline and follow up. Logistic regression models were performed to determine the associations between quartiles (using bottom quartiles as referent categories) of magnesium to iron (including total Fe, haem-Fe and non-haem Fe) ratio and the risk of IFG (>5.6 mmol/L) adjusted for covariates: age, gender, body mass index (BMI), hypertension, serum ferritin, haemoglobin and family history of diabetes.

Results

The mean (SD) intake of total Fe and magnesium was 25.0 (9.2) mg/d and 323 (125) mg/d. The incidence of IFG during 5-year follow up was 11.8%. Inverse associations were found between quartiles (Q) of Mg/haem-Fe and the risk of IFG in the fully adjusted model: odds ratios (OR) were 1.00, 0.59 (95%CI 0.35, 0.98), 0.49 (95%CI 0.28, 0.84), and 0.28 (95% CI 0.14, 0.55) (Q4), respectively. Weaker associations were found for quartiles of Mg/total Fe and no association was found between Mg/non-haem Fe and IFG risk.

Conclusions

Low Mg/haem-Fe ratio is an independent risk factor for developing IFG in Chinese adults. Future research to determine the added predictive value of assessment of low dietary Mg/haem-Fe ratio beyond current T2D risk models in specific populations is justified.

Epidemiological data showed that the number of obese people increases swiftly in all countries. Obesity can evoke metabolic syndrome or second type diabetes (T2D). So, the aim of our study was to investigate the influence of 2-[4-(benzyloxy) phenoxy] acetic acid on metabolic parameters of monosodium glutamate (MSG)-induced obesity in rats. We divided the rats as follows: 1- control group, 2 - MSG-group, 3 - MSG + 2-[4-(benzyloxy) phenoxy] acetic acid group. We investigated anthropometric parameters and blood biochemistry. It was established that MSG induced the development of visceral obesity in rats, in particular, it increased the Lee index, body mass index, deposits of subcutaneous, gonadal and visceral adipose tissue. The administration of 2-[4-(benzyloxy) phenoxy] acetic acid decreased metabolic parameters evoked by MSG. After obesity induction, there was recorded significant growth of cholesterol, triglycerides, and LDL cholesterol blood levels and significant decline in HDL cholesterol blood levels. There was a significant reduction in triglycerides, LDL cholesterol and VLDL, in 2-[4-(benzyloxy) phenoxy] acetic acid - treated group. Our results represent the basis for development of new treatment of obesity and associated conditions.

Animal models of B₁₂ deficiency have proven to be difficult due to storage of substantial amounts in the liver and the length of time required to maintain animals on a B₁₂ deficient diet to induce deficiency. Caenorhabditis elegans (C. elegans), due to its short lifespan, has recently emerged as an alternate model to investigate vitamin B12 (B12) deficiency. However, when C. elegans are maintained on bacterial diet, five generations of B12 deficient diet is required before the worms show signs of deficiency. Here we show that C. elegans grown in chemically defined axenic medium without added B12 exhibit signs of deficiency within one generation. Worms grown in deficient media had lower cobalt concentration, retarded growth, reduced fertility, increased motility, reduced quiescence and a shortened lifespan. In conclusion, C. elegans cultured in a defined axenic medium is a suitable and rapid model for studies on B12 deficiency.

Background

The major causes of hepatocellular carcinomas are Aflatoxin, hepatitis B and hepatitis C viruses.

Alpha tocopherol and its acetate and succinate esters have each been reported as counteracting cancer development in humans and rodents. We have investigated their salutary effect in both poor and high quality diets in rainbow trout Oncorhynchus mykiss as a model.

Methods

Hepatocellular carcinomas (HCCs) were induced in rainbow trout by dietary aflatoxin B1 (AfB1). A matrix of different levels of several vitamins and vitamin analogues were included in selected diets as possible anticancer agents. Identification of HCCs was made by histopathology.

Results

1.) Elevated dietary tocopheryl acetate (E-Ac) caused a marked increase in liver size and in AfB1-induced HCCs in rainbow trout. 2.) Poor diets increased the HCC incidence. 3.) Elevated dietary tocopheryl succinate (E-Su) nearly eliminated HCC development in fish fed complete diets. Tocopheryl succinate in poor diets reduced HCCs by 77% compared to tocopheryl acetate diets. 4.) Trans-retinoic acid also reduced HCC incidence. 5.) Vitamins A and D deficiency caused tumor increases but had no effect on liver size. 6.) The use of casein and dextrin in the place of soybean textured vegetable protein, in poor diets nearly eliminated the HCC risk. 7.) Trout sera showed all three vitamin forms; free α-tocopherol (E-OH), tocopheryl acetate (E-Ac) and tocopheryl succinate (E-Su), from diets containing any of these vitamin analogues, suggesting both de-esterification and trans-esterification. 8.) E-Su is discussed in the light of an anti-cancer agent that is non toxic to normal tissue but that cohorts to it are needed.

Conclusions

Increased dietary E-Ac escalated AfB1 induced HCCs and caused hepatomegaly in rainbow trout, while E-Su eliminated the HCC risk as shown by histopathology.

As obesity is now a global pandemic, greater research efforts are needed in order to fully understand the physiological effects of diets with high lipid and low carbohydrate contents, giving special attention to the factors that can lead to a condition of systemic oxidative stress. This condition is related to the onset and development of important diseases including diabetes, dyslipidemia, hypertension, stroke, and heart attack. In this work, immediately after weaning, Wistar rats (n = 8) were submitted to a hyperlipidic diet (34.5% lipids, 23.3% carbohydrates, 24.9% proteins) during 155 days. A control group (n = 8) consumed a standard diet for rodents (4.5% lipids, 48.0% carbohydrates, 25.3% proteins). The hyperlipidic diet did not cause obesity during the period of the experiment, but was detrimental to the development of mass and length of the animals during the first 57 days. A condition of oxidative stress was established, as demonstrated by decreases of plasma proteins and reduced thiols, as well as alterations of hemoglobin. Additional systemic damage was exhibited, including increased glucose intolerance and dyslipidemia, as well as hepatic damage evidenced by the plasma activities of the enzymes alanine transaminase, aspartate transaminase, and alkaline phosphatase. Decrease in lipid concentration ion white adipose tissue, which would allow increased triacylglycerol synthesis and storage if dietary carbohydrates were increased. It could be concluded that the hyperlipidic diet induced severe hepatic damage and might contribute to the future development of obesity and diabetes if the content of carbohydrates in the diet was increased.

Coenzyme Q₁₀ (CoQ₁₀) is an essential component of the mitochondrial electron transport chain responsible for different functions, among them its action as an antioxidant compound. Low CoQ₁₀ levels are related to inflammatory processes and oxidative stress, factors implicated in atherosclerosis, obesity, nonalcoholic fatty liver (NAFLD), as well as metabolic syndrome (MS). MS is a disease characterized by cardiovascular risk factors linked to obesity, dyslipidemia and hyperglycemia. NAFLD is recognized as a hepatic manifestation of MS and, together with the latter, has a high incidence in the world population. Recent investigations have underscored the positive effects of CoQ10 supplementation on the treatment of obesity, oxidative stress, MS, and NAFLD. The objective of the present study was to analyze the evidence of the effects of CoQ10 supplementation on MS and NAFLD and to provide a general view of the mechanisms of action of CoQ10 in both diseases.

Trichloromethane (TCM) serves as an ingredient in pesticide formulations and fire extinguishers. It is a reported hepato- and renal-toxin. We therefore investigated the chemo-preventive effect of diallyl disulfide (DADS) on TCM-induced hepatotoxicity. Twenty five rats, divided into five groups of five animals each were used. TCM at the dose of 200 mg/kg was orally administered, and concomitantly treated with DADS (50 mg/kg), 5 days per week for 3 weeks. Compared with control, there was a significant increase in hepatic expressions of nuclear factor kappa B (NFkB), TUNEL positive cells (apoptosis), and concentrations of malondialdehyde (MDA), hydrogen peroxide (H₂O₂), and nitric oxide (NO). Also, a significant decrease in expressions of p53, and activities of catalase (CAT) and glutathione peroxidase (GPx), as well as level of reduced glutathione (GSH) was recorded following TCM administration. Following treatment, DADS intervention significantly reduced the hepatic NFkB expressions, apoptotic positive cells as well as levels of MDA, H₂O₂, and NO, and also significantly increased the level of GSH, activities of CAT and GPx compared with TCM group, while its effect on expressions of p53 was insignificant. Hepato-protection by DADS against TCM-induced hepatotoxicity may therefore be via suppressions of NFkB activation, apoptosis, and oxidative stress in rats.

Brassica juncea, the Indian mustard variety has high erucic acid (22:1 n-9) in its oil, which causes several deleterious effects. The Centre for Genetic Manipulation of Crop Plants (India) has developed a zero-erucic and high-oleic acid transgenic mustard variety having 67% oleic acid, which is almost equivalent to that of olive oil, i.e. 71%. Therefore, we assessed its impact on erythrocyte osmotic fragility, fluidity and activities of membrane-bound enzymes and insulin sensitivity. 40 male Syrian golden hamsters of 6–8 weeks age, were divided into five groups, consisting of 8 hamsters in each and fed diet containing any one of the oils, i.e. groundnut (GNO), conventional mustard (OCM), low-erucic mustard (OLM), zero-erucic high-oleic transgenic mustard (OTM) and olive (OLO) at 10% level for 16 weeks. At the end, compared to OLO group, OTM-fed hamsters resisted osmotic shock-induced erythrocyte-haemolysis, which corroborated with higher docosahexaenoic acid (DHA; 22:6 n-3) levels in their erythrocyte membranes. However, it did affect neither the fluidity nor the activities of membrane-bound enzymes. Although fasting plasma glucose, insulin and free fatty acid levels were comparable among the various groups; during glucose challenge, OTM diet-fed animals displayed higher disposal rate of circulatory glucose, without altering the insulin levels, when compared to the conventional mustard; OCM. In conclusion, the consumption of oil from zero-erucic high-oleic transgenic mustard improved the DHA content of erythrocyte membrane, which possibly resisted haemolysis and enhanced glucose clearance during glucose overload. However, it did not affect the activities of erythrocyte membrane-bound enzymes and fluidity compared to olive oil.

The use of herb in the treatment of diseases, including nutrient-related diseases, remains the last resort in many villages. The lack of prescription for most of these herbs may negate the undoubtful efficacy of these herbs. Hence, this study seeks to propose an optimal dose of the aqueous extract of the stem bark of Theobroma cacao (TC) in the treatment of anemia and comparing the effect of this extract with that of Mangifera indica L (MI). Forty-eight weanling albino rats of both sexes (Rattus norvegicus) with a mean weight of 48.00 g ± 3.00 g were used in the study. Eight of the animals were placed on iron sufficient diet while the rest of the animals were placed on the iron deficient diet. After the four weeks, the animals were placed on iron deficient were confirmed to be iron deficient via their haematologic indexes. The iron deficient rats were then divided into nine sub groups. Each of the group of the animals was assigned different conditions for two weeks. 25, 50 and 75 mg/kg body weight of MI were administered to three of the groups. 25, 50 and 75 mg/kg body weight of TC were administered to three of the groups. A standard iron supplement drug was administered to one of the groups, the feed on one of the groups was changed to iron sufficient diet, and the last group was maintained on the iron deficient diet. The haematologic index, the intestinal disaccharidases of the animals were assayed after the treatments. The weight gained by the animal was also recorded. The iron sufficient diet and the aqueous extract from the two plants significantly increased the haematologic indexes assayed, packed cell volume, hemoglobin and red blood cell, in the animal after two weeks of administration. While increasing the dose of MI increased all the haematologic indexes in the animal, otherwise was the case for the aqueous extract of TC. Although given all the doses, the extract of MI seems to be more effective than TC, if the effect of the lowest dose, 25 mg/kg body weight is considered, TC is more effective as an anti anaemic substance than MI. The extract and iron sufficient diet also increased the activities of the intestinal lactase and sucrase in the animals. While the iron and phytochemicals in the extract seem to be acting in synergy in the increasing of the haematologic indexes, the iron content alone seems to be responsible their action on the intestinal disaccharidases. Just as proposed for MI, 25 mg/kg body weight of TC seems to be the optimal dose for the treatment.