Nutritional factors of inflammation induction or lipid mechanism of endotoxin transport

Integral parameters of bacterial lipopolysaccharide concentration and antiendotoxin immunity activity were determined in the blood serum of subjects with two extreme variants of eating disorders: obesity and anorexia nervosa (in its clinical model, long-term starvation). The results of the study showed that obese patients had initially higher endotoxin concentrations (2.41 ± 0.11 vs 1.13 ± 0.05 EU/mL in the control), which significantly decreased as a result taking a course of orlistat or after starvation (for no longer than 20 days) (to 1.34 ± 0.04 and 1.01 ± 0.09 EU/mL, respectively). The decrease in the endotoxin serum level was associated with an increase in the concentration of high-density lipoproteins (HDLs) and a decrease in the concentration of low-density lipoproteins (LDLs). This allowed us to assume that the complex of the latter with the endotoxin is the LDL fraction that may function as a depot of the hydrophobic form of the lipopolysaccharide molecule in the bloodstream. Long-term starvation (starting from day 20) led to the appearance of symptoms characteristic of septic states, which was preceded by a twofold increase in the concentration of the endotoxin and antibodies against the enterobacterial common antigen and subsequent increase in the level of anti-glycolipid antibodies (from 133.2 ± 2.6 to 355.6 ± 15.0 optical density arbitrary units) starting from day 25?C27 of starvation, which is characteristic for the initial phase of the systemic inflammatory response syndrome.     

Intestinal endotoxin in induction of type 1 diabetes

We studied serum level of intestinal flora endotoxin (LPS) in 45 children and adolescents aged 3-17 years old with diabetes mellitus type 1. Levels of endotoxin, were significantly elevated in type 1 diabetic patients (2.89 +/- 0.33 Eu/ml) compared with control (0.4 +/- 0.03 Eu/ml). There was significant difference in serum LPS levels in patients with type 1 diabetes onset (3.93 +/- 0.79 Eu/ml) compared with children and adolescent with old time diabetes (2.37 +/- 0.27 Eu/ml). These results have a major implication on our understanding of the role of gut flora endotoxin in pathogenesis of type 1 diabetes.     

Atherothrombosis and oxidative stress: the connection and correlation in diabetes

Abstract

Background: Hyperglycaemia-induced depletion of reduced glutathione (GSH) causes erythrocyte oxidative stress (EOS), which leads to vascular events including exacerbation of thrombotic events evidenced by changes in D-dimer level. It would, therefore, appear that there is a complex link between GSH and D-dimer, which are part of an emerging array of biomarkers associated with diabetes. The objective of this study was to investigate evidence of correlation between levels of plasma D-dimer and erythrocyte GSH in diabetes disease progression.

Subjects and methods: A cohort of 69 subjects were selected based on medical history plus clinical findings and equally divided into control, prediabetes and diabetes groups, matched for age and sex. Plasma D-dimer and erythrocyte reduced glutathione (GSH) were determined and separated into quartiles as a means of indicating disease severity. Statistical analysis was by Pearson's correlation coefficient.

Results: Of the three groups, only the diabetes group showed any correlation between GSH and D-dimer. Of importance is that for increasing GSH, the second quartile range of GSH (xbar ± SD = 45 ± 22 mg/100ml) showed a statistically significant negative correlation for ranked D-dimer (xbar ± SD = 1055 ± 828 μg/l; r = ?0.88; P < 0.02). The fourth quartile GSH range (xbar ± SD = 79 ± 40 mg/100 ml) showed a statistically significant positive correlation with D-dimer (xbar ± SD = 1055 ± 828 μg/l; r = 0.91; P < 0.02). Thus, within the diabetes group only, the increasing level of oxidative stress as measured by GSH first indicates a reduction in D-dimer followed by a rise in D-dimer, which led to the proposal of a two-part process of atherosclerosis that reconciles previous contradictory findings.

Conclusions: This study provides not only evidence of a correlation between oxidative stress level and fibrinolysis in diabetes, but also an explanation of why previous studies have found both hypo- or hyperfibrinolysis associated with diabetes.     

Beneficial effects of soy protein in the initiation and progression against dimethylbenz [a] anthracene-induced breast tumors in female rats

Objective: Although recent studies link altered cellular redox state to protein dysfunction in various disease-states, such associations are least studied in clinical diabetes. Therefore, this study assessed the levels of reduced glutathione (GSH) and Na⁺/K⁺ ATPase activities in type 2 diabetic patients with and without microangiopathy. Methods: The study group comprised of a total of 160 subjects, which included non-diabetic healthy controls (n = 40) and type 2 diabetic patients without (n = 60) and with microangiopathy (n = 60), defined as presence of retinopathy with or without nephropathy. Erythrocyte Na⁺/K⁺ ATPase activity and GSH levels were estimated spectrophotometrically and fluorometry was used to determine the plasma thiobarbituric acid reactive substances (TBARS) and serum advanced glycation end products (AGEs). Results: GSH levels in diabetic subjects without (4.8± 0.15 μmol/g Hb) and with microangiopathy (5.2± 0.14 μmol/g Hb) were significantly lower (p < 0.001) compared to control subjects (6.3± 0.14 μmol/g Hb). Erythrocyte Na⁺/K⁺ ATPase activity was significantly reduced (p < 0.001) in diabetes subjects with (272± 7 nmol Pi/mg protein/h) and without microangiopathy (304 ± 8) compared to control (374 ± 6) subjects. TBARS were significantly higher (p < 0.001) in diabetes subjects with (10.65± 0.81 nM/ml) and without microangiopathy (9.90± 0.5 nM/ml) compared to control subjects (5.18± 0.18 nM/ml). Advanced glycation end product levels were also significantly (p < 0.001) elevated in diabetic subjects with microangiopathy (8.2± 1.8 AU) when compared to diabetes subjects without microangiopathy (7.0± 2.0 AU) and control subjects (4.6± 1.9 AU). On multivariate regression analysis, GSH levels showed a positive association with the Na⁺/K⁺ ATPase activity and negative association with TBARS and AGE levels. Conclusion: Hypoglutathionemia and increased oxidative stress appears to be early biochemical aberrations in diabetes, and through protein alterations, oxidative stress and redox modifications may contribute to pathogenesis of diabetic microangiopathy.     

Ubiquinone-10 plasma concentrations in healthy European children

The reduced form of ubiquinone-10 (coenzyme Q) has been shown to represent an important physiologic antioxidant principle in human blood. In order to establish a reference range for infants, we measured plasma levels of ubiquinone in 50 healthy European children aged 2 months to 15 years. A mean ±SD) value of 0.75±0.27 μg/ml plasma (0.87±0.31 μM) was determined; ubiquinone concentrations were not found to be sex-dependent (0.7±0.24μg/ml for girls, n=17, and 0.7±0.28μg/ml for boys, n=33) but correlated negatively with age (r = -0.37, P=0.0075). This negative correlation was mainly due to relatively high levels in infants approximately 1 year old.

The mean value determined does not significantly differ from the average ubiquinone plasma concentrations determined in healthy Nigerian children (0.85±0.40 μg/ml, n= 18) in a previous study (Becker K, Boetticher D, Leichsenring M. Internat J Vitam Nutr Res 1995, in press).     

Reduced Levels of Brain Derived Neurotrophic Factor (BDNF) in the Serum of Diabetic Retinopathy Patients and in the Retina of Diabetic Rats

Diabetic retinopathy (DR) is widely recognized as a neurovascular disease. Retina, being a neuronal tissue of the eye, produces neurotrophic factors for its maintenance. However, diabetes dysregulates their levels and thereby may damage the retina. Among neurotrophins, brain derived neurotrophic factor (BDNF) is the most abundant in the retina. In this study, we investigated the level of BDNF in the serum of patients with DR and also in the serum and retina of streptozotocin-induced diabetic rats. The level of BDNF was significantly decreased in the serum of proliferative diabetic retinopathy patients as compared to that of non-diabetic healthy controls (25.5 ± 8.5–10.0 ± 8.1 ng/ml, p < 0.001) as well as compared to that of diabetic patients with no retinopathy (21.8 ± 4.7–10.0 ± 8.1 ng/ml, p < 0.001), as measured by ELISA techniques. The levels of BDNF in the serum and retina of diabetic rats were also significantly reduced compared to that of non-diabetic controls (p < 0.05). In addition, the expression level of tropomyosin-related kinase B (TrkB) was significantly decreased in diabetic rat retina compared to that of non-diabetic controls as determined by Western blotting technique. Caspase-3 activity was increased in diabetic rat retina after 3 weeks of diabetes and remained elevated until 10 weeks, which negatively correlated with the level of BDNF (r = ?0.544, p = 0.013). Our results indicate that reduced levels of BDNF in diabetes may cause apoptosis and neurodegeneration early in diabetic retina, which may lead to neuro-vascular damage later in DR.     

Salivary Nickel and Chromium Levels in Orthodontic Patients with and Without Periodontitis: a Preliminary Historical Cohort Study

Many periodontal patients may need orthodontic treatment. Alterations in oral environment particularly the reduction of pH in periodontal patients could affect metal ion release from orthodontic appliances. However, there is no study on metal ion release in periodontal patients. The aim of this preliminary study was to comparatively evaluate, for the first time, salivary levels of nickel and chromium in periodontal patients (versus healthy controls) under orthodontic treatment for 2 months. In this in vivo study, 40 subjects were evaluated. Patient selection and standardization of orthodontic treatment protocols were prospectively designed and performed. Two groups of n = 20 each (control: healthy orthodontic patients, cohort: orthodontic patients with periodontitis) underwent similar protocols of fixed orthodontic treatment for 2 months. After 2 months, salivary nickel and chromium concentrations of the case and cohort groups were measured using inductively coupled plasma mass spectrometry (ICP-MS). The values were compared between the two groups using t test. There were 10 men and 10 women in each group. The mean age of patients was 34.6 ± 3.6 years old. The salivary level of nickel was 338.2 ± 235.5 ng/ml and 182.8 ± 116.5 ng/ml in the cohort and control groups, respectively (P = 0.0118). The salivary level of chromium was 7.4 ± 3.15 ng/ml in the cohort and 6.35 ± 2.39 ng/ml in the control group (P = 0.2214). Salivary level of nickel might be considerably higher in periodontal patients undergoing 2 months of orthodontic treatment compared to orthodontic patients with healthy gingivae.

     

Serum sulfatides as a novel biomarker for cardiovascular disease in patients with end-stage renal failure

Sulfatides, normal components of serum lipoproteins, may play an important role in cardiovascular disease due to their various modulatory functions in haemostasis. The incidence of cardiovascular disease in patients with end-stage renal failure undergoing maintenance hemodialysis has been reported to be approximately 10 to 30 times higher than that in the general population. To elucidate the possible roles of serum sulfatides in this high incidence, we measured the level of sulfatides in 59 such patients, by converting them to lysosulfatides according to a recently developed quantitative, qualitative, high-throughput technique using matrix-assisted laser desorption ionization-time of flight mass spectrometry. The mean level of sulfatides in patients 3.58 ± 1.18 nmol/ml was significantly lower than that in age-matched normal subjects (8.21 ± 1.50 nmol/ml; P < 0.001). Patients receiving maintenance hemodialysis over a longer period had lower levels of sulfatides. When the mean levels of sulfatides were compared between patients with cardiovascular disease (N = 22) and those without the disease (N = 37), the level in the former group 2.85 ± 0.67 nmol/ml was found to be significantly lower than that in the latter group 4.01 ± 1.22 nmol/ml (P < 0.001). These findings reveal a close correlation between low levels of serum sulfatides and a high risk of cardiovascular disease in these patients. Determination of the level of serum sulfatides can contribute to predictions of the incidence of cardiovascular disease in patients with end-stage renal failure undergoing maintenance hemodialysis.     

Plasma visfatin concentration as a surrogate marker for visceral fat accumulation in obese children

Objective: This study was designed to elucidate whether the plasma visfatin level reflects visceral or subcutaneous fat accumulation and metabolic derangement in obese children. Methods and Procedures: Fifty‐six obese Japanese children, including 37 boys and 19 girls were enrolled in the study. The age of the subjects ranged from 5 to 15 (10.2 ± 0.3; mean ± s.e.m.) years. The age‐matched control group for measuring visfatin consisted of 20 non‐obese children. Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) areas were measured by computed tomography. The plasma concentrations for visfatin and leptin were assayed by enzyme‐linked immunosorbent assay kits. Results: The plasma visfatin level was higher in the obese (14.7 ± 0.9 ng/ml) than in the control children (8.6 ± 0.6 ng/ml). In a univariate analysis, the visfatin correlated significantly with age, height, body weight, waist circumference, VAT and SAT area, triglyceride (TG), insulin, and the homeostasis model assessment for insulin resistance (HOMA‐R). After being adjusted for age and sex, only the VAT area retained significant partial correlation with visfatin, and in contrast the body weight, BMI–s.d., and SAT area with leptin. The plasma visfatin concentration was not correlated with leptin. The plasma visfatin levels in the control, non‐metabolic syndrome (MS) (n = 49), and MS groups (n = 7) were significantly different from each other. Discussion: These results suggest that plasma visfatin level is a specific marker for visceral fat accumulation in obese children. As a good surrogate marker, plasma visfatin level can predict the VAT area in obese children.     

Establishment of Radioimmunoassay for Human Macrophage Colony-stimulating Factor Using Recombinant Human Macrophage Colony-stimulating Factor as Tracer and Immunogen

A sensitive and reliable radioimmunoassay (RIA) for human macrophage colony-stimulating factor (M-CSF) was developed using recombinant human M-CSF (rhM-CSF) as tracer and immunogen. The assay was quantitative over the range of 50 pg/ml and 5.0 ng/ml for M-CSF in human urine and serum, and more sensitive and specific than the murine bone marrow assay. The average level of human M-CSF in urine from normal males (N = 71) and females (N = 46) was 3.94 ± 1.78 ng/ml (2.85 ± 1.15 μg/g creatinine), and 3.53 ± 1.70ng/ml (3.31 ± 1.12 μg/g creatinine), respectively. The serum levels were 1.95 ± 0.38ng/ml for males (N = 117), and 1.93 ± 0.49 ng/ml for females, (N = 16). The results with the urine and sera showed that there was no difference in the M-CSF levels due to age or gender.     

Confirmation of Superoxide Generation via Xanthine Oxidase in Streptozotocin-induced Diabetic Mice

Reactive oxygen species (ROS) may play key roles in vascular inflammation and atherogenesis in patients with diabetes. In this study, xanthine oxidase (XO) system was examined as a potential source of superoxide in mice with streptozotocin (STZ)-induced experimental diabetes. Plasma XO activity increased 3-fold in diabetic mice (50±33?μU/ml) 2 weeks after the onset of diabetes, as compared with non-diabetic control mice (15±6?μU/ml). In vivo superoxide generation in diabetic mice was evaluated by an in vivo electron spin resonance (ESR)/spin probe method. Superoxide generation was significantly enhanced in diabetic mice, and the enhancement was restored by the administration of superoxide dismutase (SOD) and 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron), which was reported to scavenge superoxide. Pretreatment of diabetic mice with XO inhibitors, allopurinol and its active metabolite oxipurinol, normalized the increased superoxide generation. In addition, there was a correlation (r=0.78) between the level of plasma XO activity and the relative degree of superoxide generation in diabetic and non-diabetic mice. Hence, the results of this study strongly suggest that superoxide should be generated through the increased XO seen in the diabetic model mice, which may be involved in the pathogenesis of diabetic vascular complications.     

Relationships between COL2A1 gene polymorphisms and knee osteoarthritis in Han Chinese women

To investigate the relationships between two COL2A1 single nucleotide polymorphisms (SNPs; T2088C and G4006A) and osteoarthritis (OA) in Han Chinese women. One hundred and twenty OA women and 120 control women were recruited. Genomic DNA was extracted from the whole blood. The COL2A1 polymorphisms T2088C and G4006A were analyzed by TaqMan assay. The levels of plasma N-propetide of type IIA collagen (PIIANP) and urinary C-telopeptide of type IIA collagen (CTX-II) were determined by ELISA. The level of plasma PIIANP significantly decreased in the OA group, compared with that in the control group (P < 0.05), with 15.6 ± 4.2 ng/ml (Mean ± SD) in the OA group and 30.2 ± 7.8 ng/ml in the control group. The level of urinary CTX-II significantly increased in the OA group, compared with that in the control group (P < 0.05), with 201.4 ± 10.2 ng/ml in the control group and 250.8 ± 15.6 ng/ml in the OA group. There was no difference in the T2088C genotypes between the OA and control groups. The G4006A AA homozygous genotype significantly increased in the OA patients, when compared with that in the control women (P < 0.05, χ²), with 24.2% (29/120) in the OA group and 10.0% (12/120) in the control group; The A allele accounted for 49.2% (118/240) in the OA group and 35.8% (86/240) in the control group. Among the G4006A genotypes, the plasma PIIANP level of the AA genotype (16.4 ± 6.6 ng/ml) was significantly lower than those of the GG genotype (28.6 ± 4.2 ng/ml) and GA genotype (21.5 ± 8.0 ng/ml) while the urinary CTX-II level of the AA genotype (255.2 ± 18.4 ng/ml) significantly increased, compared with those of the GG genotype (218.4 ± 13.2 ng/ml) and GA genotype (221.2 ± 15.6 ng/ml). The haplotype analysis shows that T-G was a protective factor for OA and that T-A was a risk factor. The AA genotype, A allele and T-A may increase the risk of OA in the Han Chinese women while T-G may protect these women from OA.     

Human Melatonin and Cortisol Circadian Rhythms in Patients with Coronary Heart Disease

Cortisol and melatonin have well known circadian rhythms, coupled to the solar day. Melatonin has been shown to serve as an endogenuous “Zeitgeber” (time giver) and is secreted by the human pineal gland throughout the night but not during the day. Patients with coronary heart disease (CHD) have significant depressed nocturnal melatonin secretion compared to healthy individuals (Brugger et al., 1995). In addition to our previous study we measured serum concentrations of cortisol to evaluate whether the circadian rhythm of cortisol secretion is also different in patients with CHD. Blood was collected by venous puncture at 0200 and at 1400, serum separated and kept frozen at -20°C until analysis. Cortisol and melatonin were measured with a commercially available radioimmunoassay according to the instructions of the manufacturer. Nineteen patients with angiographically documented CHD (mean age 53 years) participated in this study. As control group served 12 adults without any signs of CHD. Melatonin serum concentrations (median; mean ± SD) at night were significantly depressed in patients with coronary heart disease (7.8; 8.6 ± 3.3 pg/ml) in comparison to the control group (38.0; 45.4 ± 24.1 pg/ml) p &lt; 0.01. Melatonin in the afternoon was not detectable in either of the groups. Cortisol values at night were significantly raised in patients with coronary heart disease (6.0; 7.2 ± 3.7 µg/dl) in comparison to the control group (2.7; 3.8 ± 2.9 µg/dl) p &lt; 0.05. Cortisol levels in the afternoon were also elevated in patients with CHD (8.9; 9.5 ± 3.8 µg/dl) but there was no significant difference compared to controls (6.8; 6.9 ± 4.5 µg/dl). The results of the present study indicate that patients with coronary heart disease have atypical secretory patterns of nocturnal cortisol and melatonin secretion.     

Teniasis

The aim of this study was to investigate the changes of level of the essential elements of copper, magnesium, and zinc status in cases of teniasis in children. Copper, magnesium, and zinc levels were measured in 40 children who were positive for intestinal parasite of Taenia saginata. Scores were obtained for the positives and their 30 age- and sex-matched T. saginata-negative healthy children. The mean concentration of copper, magnesium, and zinc in blood showed no statistically difference in T. saginata-positive children than in their controls both in females (p>0.05) and males (p>0.05). However, a clear numerically decrease was observed especially in magnesium and zinc levels compared to the controls both in females and males. The average magnesium concentration in T. saginata-positive female children and male children were 20±1.9 and 22±2.2 mg/L and it was 27±2.1 and 27±2.3 mg/L in controls, respectively. The mean values of the zinc in blood were 0.76±0.5 and 0.72±0.4 mg/L in T. saginata-positive female children and male children and 0.85±0.3 and 0.81±0.5 mg/L in female and male controls, respectively. No correlation could be demonstrated between age and mean values of copper, magnesium, and zinc in T. saginata-positive females and males and controls (p>0.05). No significant correlation could be found between blood copper, magnesium and zinc levels in T. saginata-positive female and male children and controls (p>0.05). Although there was no statistical correlation observed in copper, magnesium, and zinc levels between patients and controls, there seem to be, especially in magnesium and zinc levels, a decrease, whereas no change was seen in the zinc level in children infected with T. saginata compared to controls.     

Gonadal development and steroid hormone profile of wild caught grey mullet (Mugil cephalus)

The grey mullet Mugil cephalus is one of the popular and fast growing fishes being cultured in tropical and subtropical regions. In the present study, histological observation of gonadal development and corresponding changes in sex steroid levels from different maturity stages of wild caught male and female were studied. In female, testosterone and 17β-estradiol increased with the advancement of maturation and reached peak (17β-estradiol, 323 ± 13 pg/ml; testosterone, 938 ± 7.87 pg/ml) in mature stage, whereas the level of progesterone was maximum (488 ± 4.9 pg/ml) during ripe stage. Vitellogenin level in serum showed a similar trend as 17β-estradiol. In case of male, the testosterone level in serum increased gradually with advancement of maturation and was maximum (1820 ± 40.25 pg/ml) during ripe stage, whereas significant decrease in 17β-estradiol and progesterone was noticed with advancement of maturation. The fundamental information from this investigation would be useful for developing protocol for accelerating maturation and spawning under captive condition.     

Maternal Influence,Not Diabetic Intrauterine Environment,Predicts Children's Energy Intake

Offspring of women with diabetes during pregnancy are at increased risk of accelerated weight gain and diabetes, effects partly mediated by the in utero environment. Whether differences in energy intake can explain this increased risk is unknown. We compared diet composition, eating patterns, and physiological responses to a mixed meal in 63 nondiabetic children whose mothers developed diabetes either before (offspring of diabetic mothers, ODMs, n = 31, age 9.2 ± 1.7 years, mean ± s.d.) or after (offspring of prediabetic mothers, OPDMs, n = 32, 9.6 ± 1.3 years) the pregnancy. After consuming a standardized diet for 3 days, participants ate ad libitum from a computer‐operated vending machine stocked with foods they had rated favorably on a food preferences questionnaire. Mothers and children always ate together. A subset of 35 children underwent a meal test with blood draws to measure insulin and glucose. Children's energy intake was associated with age, sex, and percent body fat, and strongly with mother's energy intake (r = 0.57, P < 0.0001). After adjustment for these variables, there were no differences between ODM and OPDM in energy intake or diet composition. The insulin area under the curve (AUC) following the meal test was significantly correlated with total energy intake but not after adjustment for the above covariates. Differences in energy intake were not observed between ODM and OPDM. Mother's energy intake was a significant predictor of children's energy intake. These findings indicate that in this subset of children in a controlled in‐patient setting, maternal influence may outweigh intrauterine effects on energy intake.     

Altered Intramuscular Lipid Metabolism Relates to Diminished Insulin Action in Men,but Not Women,in Progression to Diabetes

Whether sex differences in intramuscular triglyceride (IMTG) metabolism underlie sex differences in the progression to diabetes are unknown. Therefore, the current study examined IMTG concentration and fractional synthesis rate (FSR) in obese men and women with normal glucose tolerance (NGT) vs. those with prediabetes (PD). PD (n = 13 men and 7 women) and NGT (n = 7 men and 12 women) groups were matched for age and anthropometry. Insulin action was quantified using a hyperinsulinemic‐euglycemic clamp with infusion of [6,6^?2H₂]‐glucose. IMTG concentration was measured by gas chromatography/mass spectrometry (GC/MS) and FSR by GC/combustion isotope ratio MS (C‐IRMS), from muscle biopsies taken after infusion of [U^?13C]palmitate during 4 h of rest. In PD men, the metabolic clearance rate (MCR) of glucose was lower during the clamp (4.71 ± 0.77 vs. 8.62 ± 1.26 ml/kg fat‐free mass (FFM)/min, P = 0.04; with a trend for lower glucose rate of disappearance (Rd), P = 0.07), in addition to higher IMTG concentration (41.2 ± 5.0 vs. 21.2 ± 3.4 µg/mg dry weight, P ≤ 0.01), lower FSR (0.21 ± 0.03 vs. 0.42 ± 0.06 %/h, P ≤ 0.01), and lower oxidative capacity (P = 0.03) compared to NGT men. In contrast, no difference in Rd, IMTG concentration, or FSR was seen in PD vs. NGT women. Surprisingly, glucose Rd during the clamp was not different between NGT men and women (P = 0.25) despite IMTG concentration being higher (42.6 ± 6.1 vs. 21.2 ± 3.4 µg/mg dry weight, P = 0.03) and FSR being lower (0.23 ± 0.04 vs. 0.42 ± 0.06 %/h, P = 0.02) in women. Alterations in IMTG metabolism relate to diminished insulin action in men, but not women, in the progression toward diabetes.     

Visceral obesity is a negative predictor of remission of diabetes 1 year after bariatric surgery

Our aim was to identify preoperative anthropometric and clinical parameters that predict the remission of diabetes after Roux‐en‐Y gastric bypass (RYGB). Fifty severely obese Korean patients with type 2 diabetes underwent RYGB. Visceral and abdominal subcutaneous fat area (SFA) was assessed using computed tomography before and 6 and 12 months after RYGB. Remission was defined as a glycated hemoglobin (A_1C) level <6.5% and a fasting glucose concentration <126 mg/dl for 1 year or more without the use of medication. The visceral‐to‐SFA ratio decreased from 0.60 ± 0.30 to 0.53 ± 0.29 (P = 0.001) after 6 months and decreased further to 0.42 ± 0.24 (P < 0.001) after 12 months. Thirty‐four of the 50 patients (68%) had remission of diabetes (remission group). Compared with patients in the nonremission group, patients in the remission group had a shorter duration of diabetes and lower preoperative A_1C level, and were less likely to use insulin preoperatively. Preoperative BMI did not differ in two groups. However, the preoperative visceral‐to‐SFA ratio was greater in the nonremission group compared with the remission group (0.79 ± 0.29 vs. 0.53 ± 0.26, P = 0.003). Finally, the preoperative visceral‐to‐SFA ratio was an independent predictor of the remission of diabetes after RYGB in multiple stepwise logistic regression analysis. In conclusion, our data suggest that visceral adiposity negatively influence the likelihood of the patient experiencing the remission of diabetes after RYGB.     

Energy Intake and Meal Portions: Associations with BMI Percentile in U.S. Children

Objective: We examined relationships of eating patterns and reported energy intake (rEI) with BMI percentile in U.S. children. Research Methods and Procedures: Two 24‐hour dietary recalls from the Continuing Surveys of Food Intakes by Individuals 1994 to 1996 and 1998 (1005 boys, 990 girls) were averaged, and children were categorized into three age groups: 3 to 5 years (n = 1077), 6 to 11 years (n = 537), and 12 to 19 years (n = 381). Physiologically implausible reports due to reporting bias or abnormal intake (rEI outside ±18% to 23% of predicted energy requirements; pER) were identified. Results: rEI averaged 109 ± 34% and 100 ± 10% of pER in the total and plausible samples, respectively. EI was overreported more in younger children and underreported more in overweight older children. Children with plausible rEI (45.3% of sample) averaged 4.7 eating occasions/d, 589 kcal/meal, 223 kcal/snack, and 2038 kcal/d. rEI was not associated with BMI percentile in the total sample. In the plausible sample, rEI, meal portion size, and meal energy were positively associated with BMI percentile in boys 6 to 11 years and in children 12 to 19 years. No relationships were found in children 3 to 5 years and girls 6 to 11 years. Relationships were more consistent and stronger in the plausible compared with the total sample. Discussion: Excluding implausible dietary reports may be necessary for discerning dietary associations with BMI percentile. EI and meal, but not snack, patterns may play a quantitatively greater role in weight regulation as children age.     

Aerobic capacity of Peruvian Quechua: A test of the developmental adaptation hypothesis

High altitude natives are reported to have outstanding work capacity in spite of the challenge of oxygen transport and delivery in hypoxia. To evaluate the developmental effect of lifelong exposure to hypoxia on aerobic capacity, VO_2peak was measured on two groups of Peruvian Quechua subjects (18–35 years), who differed in their developmental exposure to altitude. Male and female volunteers were recruited in Lima, Peru (150 m), and were divided in two groups, based on their developmental exposure to hypoxia, those: a) Born at sea‐level individuals (BSL), with no developmental exposure to hypoxia (n = 34) and b) Born at high‐altitude individuals (BHA) with full developmental exposure to hypoxia (n = 32), but who migrated to sea‐level as adults (>16‐years‐old). Tests were conducted both in normoxia (BP = 750 mm Hg) and normobaric hypoxia at sea‐level (BP = 750 mm Hg, FiO₂ = 0.12, equivalent to 4,449 m), after a 2‐month training period (in order to control for initial differences in physical fitness) at sea‐level. BHA had a significantly higher VO_2peak at hypoxia (40.31 ± 1.0 ml/min/kg) as compared to BSL (35.78 ± 0.96 ml/min/kg, P = 0.001), adjusting for sex. The decrease of VO_2peak at HA relative to SL (ΔVO_2peak) was not different between groups, controlling for baseline levels (VO_2peak at sea‐level) and sex (BHA = 0.35 ± 0.04 l/min, BSL = 0.44 ± 0.04 l/min; P = 0.12). Forced vital capacity (controlling for height) and the residuals of VO_2peak (controlling for weight) had a significant association in the BHA group only (r = 0.155; P = 0.031). In sum, results indicate that developmental exposure to altitude constitutes an important factor to determine superior exercise performance. Am J Phys Anthropol 156:363–373, 2015. © 2014 Wiley Periodicals, Inc.