Declines in TBT contamination in Irish coastal waters 1987-2011, using the dogwhelk (Nucella lapillus) as a biological indicator.

Using the vas deferens sequence index (VDSI) and relative penis size index (RPSI) in dogwhelks (Nucella lapillus), imposex levels were assessed at 63 sites within 11 sea inlets during 2010/2011 and compared these with levels gathered since 1987. Sterile females (VDS>5.0) were found at 14 of the 63 sites and 47 sites (75%) met the EcoQO (VDSI<2.0). The absence of imposex in 'control' areas on the west coast is due to the lack of vessel paint applications or net dips with TBT being used as an active anti-fouling ingredient. A significant decline was observed following 2005 when comparing VDSI levels which is consistent with the decline of TBT usage. Current levels are consistent with an overall improvement towards achieving Good Environmental Status according to the requirements under the Marine Strategy Framework Directive.

Sporadic Cryptosporidium infection in Nigerian children: risk factors with species identification.

A cross-sectional study was conducted to investigate risk factors for sporadic Cryptosporidium infection in a paediatric population in Nigeria. Of 692 children, 134 (19·4%) were infected with Cryptosporidium oocysts. Cryptosporidium spp. were identified in 49 positive samples using PCR-restriction fragment length polymorphism and direct sequencing of the glycoprotein60 (GP60) gene. Generalized linear mixed-effects models were used to identify risk factors for all Cryptosporidium infections, as well as for C. hominis and C. parvum both together and separately. Risk factors identified for all Cryptosporidium infections included malaria infection and a lack of Ascaris infection. For C. hominis infections, stunting and younger age were highlighted as risk factors, while stunting and malaria infection were identified as risk factors for C. parvum infection.

Muscle insulin receptor concentrations in obese patients post bariatric surgery: relationship to hyperinsulinemia.

OBJECTIVE: Obesity results in insulin resistance. Bariatric surgery for obese individuals induces weight loss, improves insulin sensitivity, and lowers insulin levels. We investigated the mechanisms of this improvement. DESIGN: Insulin receptor (IR) content, IR signaling, and adiponectin levels were measured in nine morbidly obese subjects before and after bariatric surgery. SUBJECTS: Seven female and two male, average age 44+/-2y, BMI >40 kg/m(2) and/or at least 100 lbs over ideal body weight, undergoing elective bariatric surgery. MEASUREMENTS: Before surgery BMI, fasting plasma glucose, adiponectin, and insulin levels were measured. A fasting muscle biopsy was obtained from the vastus lateralis for IR concentration and autophosphorylation activity measurements. These procedures were repeated 1 y after surgery. RESULTS: At 1 y after surgery, the subjects had lost an average of 48.3+/-5.6 kg (P<0.001), insulin sensitivity had significantly increased as determined by the minimal model (SI 0.72+/-0.18 vs 3.86+/-1.43, P<0.05), and IR content had increased two-fold in muscle (2.1+/-0.4 vs 4.3+/-0.7 ng/mg protein, P<0.01). The increase in IR content was related to fasting insulin levels. In the subjects with the lowest IR function, there was also an increase in IR function. Plasma adiponectin increased by 40% following weight loss (7.4+/-1.6 pre vs 10.3+/-1.3 mg/ml post, P<0.05). There was no significant change in muscle content of the IR inhibitor, PC-1. CONCLUSION: Increased IR content, most likely regulated by insulin levels, may be one contributor to the increased insulin sensitivity that occurs when morbidly obese patients undergo bariatric surgery.

Plasma cholesteryl ester transfer protein activity is not linked to insulin sensitivity.

Plasma cholesteryl ester transfer protein (CETP) activity has been reported to decline during a hyperinsulinemic-euglycemic clamp. It has been suggested that this suppressive effect of acute hyperinsulinemia is linked to whole body insulin sensitivity, and that the insulin resistance that accompanies obesity leads to high plasma CETP activity found in obese subjects. In the present study, we used 2 experimental approaches to examine the putative link between CETP and insulin action. First, we examined if the clamp-induced suppression of plasma CETP activity is linked to whole body insulin sensitivity. Plasma CETP activity was measured at the beginning and end of a 2-hour hyperinsulinemic-euglycemic clamp in 18 nondiabetic individuals before and after an exercise training regimen that improved insulin sensitivity without weight loss. CETP activity decreased in response to the clamp procedure in 16 of 18 subjects, and on average, by 9% (P <.001). While training decreased plasma CETP activity (10%, P <.05), the improvement in insulin sensitivity had no statistical effect on the clamp-induced suppression of plasma CETP activity (training*clamp, P =.26). Second, we examined if insulin resistance is associated with an elevation in fasting plasma CETP activity when the influence of adiposity and diabetes were negated. Plasma CETP activity was measured in 41 women (12 insulin-sensitive lean; 8 insulin-resistant lean; 10 insulin-sensitive obese; 11 insulin-resistant obese). The level of insulin sensitivity had no significant effect on fasting plasma CETP activity, but CETP levels were 25% higher in obese subjects (P <.01). Thus, neither experimental approach provided evidence that plasma CETP levels are linked to insulin and insulin sensitivity. These data suggest that the elevated CETP activity found in obese patients is less associated with hyperinsulinemia and the accompanying insulin resistance, but rather is more related to some other metabolic complication of obesity.

Effect of intense training on plasma leptin in male and female swimmers.

PURPOSE: The purpose of this study was to determine whether fasting plasma leptin concentration was altered with an increase in training volume in competitive male and female athletes. METHODS: Intercollegiate male (N = 9) and female (N = 12) swimmers were examined during the preseason and at two times during the mid-season (mid-season 1 and mid-season 2) when training volume was relatively high (33,000 m.wk(-1)). Body composition (hydrostatic weighing), energy intake and expenditure, and fasting plasma leptin concentration were measured. RESULTS: In the women, there was a significant (P < 0.05) decline in fat mass (2 kg) with the increase in training volume, which was not accompanied by a reduction in fasting leptin (12.8 +/- 1.5 vs 11.0 +/- 1.2 vs 11.0 +/- 1.5 ng.mL(-1) for preseason, mid-season 1, and mid-season 2, respectively). In the men, there were no significant changes in body composition, body mass, or fasting leptin (4.4 +/- 0.8 vs 4.3 +/- 0.8 vs 4.6 +/- 0.8 ng.mL(-1), respectively). CONCLUSION: These findings suggest 1) plasma leptin is not sensitive to an increase in training volume and 2) leptin may not be indicative of changes in fat mass with an increase in training volume in female athletes. These data suggest that leptin may not be useful in monitoring relative training stress in athletes.

Enhanced muscle insulin receptor autophosphorylation with short-term aerobic exercise training.

Exercise training improves insulin action in skeletal muscle, but the mechanisms of this effect are not completely understood. In particular, the role of the insulin receptor (IR) is unclear. We examined the IR and an enzyme indicative of oxidative capacity in muscle in relation to improved insulin action in 20 previously sedentary individuals before and after a 7-day program of moderate-intensity cycle ergometry. After training, insulin sensitivity increased 33% (6.20 +/- 0.91 vs. 8.22 +/- 1.12 min. microU(-1). ml(-1) mean +/- SE, pre- vs. posttraining, respectively, P < 0.05). The mitochondrial marker enzyme cytochrome c oxidase (COX) increased in vastus lateralis biopsies by 21% (P < 0.05). After training, IR autophosphorylation, determined by ELISA, was significantly increased by approximately 40% at insulin concentrations from 1 to 100 nM (P < 0.05). The training-induced improvements in IR autophosphorylation were significantly correlated with changes in muscle COX content (r = 0.65, P < 0.05). These studies indicate that, in this model of increased physical activity, improvements in IR function are an early adaptation to exercise in humans, are correlated with increases in muscle oxidative capacity, and likely contribute to the beneficial effects of exercise training on insulin action.

Effect of short-term exercise training on insulin-stimulated PI 3-kinase activity in human skeletal muscle.

The purpose of this study was to determine if the improvement in insulin sensitivity with exercise training is associated with enhanced phosphatidylinositol 3-kinase (PI 3-kinase) activity. Nine sedentary men were studied before and after 7 days of exercise training (1 h/day, approximately 75% maximal oxygen consumption). Insulin sensitivity was determined with a euglycemic-hyperinsulinemic glucose clamp in the sedentary state and 15-17 h after the final exercise bout. PI 3-kinase activity was determined from samples (vastus lateralis) obtained in the fasted condition and after 60 min of submaximal insulin stimulation during the clamp. After exercise, glucose infusion rate increased (P < 0. 05) significantly (means +/- SE, 7.8 +/- 0.5 vs. 9.8 +/- 0.8 mg. kg(-1). min(-1)), indicating improved insulin sensitivity. Insulin-stimulated (insulin stimulated/fasting) phosphotyrosine immunoprecipitable PI 3-kinase activity also increased significantly (P < 0.05) with exercise (3.1 +/- 0.8-fold) compared with the sedentary condition (1.3 +/- 0.1-fold). There was no change in fasting PI 3-kinase activity. These data suggest that an enhancement of insulin signal transduction in skeletal muscle may contribute to the improvement in insulin action with exercise.

Insulin activation of phosphatidylinositol 3-kinase in human skeletal muscle in vivo.

The purpose of this investigation was to determine whether insulin-stimulated phosphatidylinositol 3-kinase (PI3-kinase) activity is detectable in needle biopsies of human skeletal muscle. Sixteen healthy nonobese males matched for age, percent fat, fasting insulin, and fasting glucose participated in one of two experimental protocols. During an intravenous glucose tolerance test (IVGTT) protocol, insulin-stimulated PI3-kinase activity was determined from percutaneous needle biopsies at 2, 5, and 15 min post-insulin administration (0.025 U/kg). In the second group, a 2-h, 100 mU . m-2 . min-1 euglycemic hyperinsulinemic clamp was performed, and biopsies were obtained at 15, 60, and 120 min after insulin infusion was begun. Insulin stimulated PI3-kinase activity by 1.6 +/- 0.2-, 2. 2 +/- 0.3-, and 2.2 +/- 0.4-fold at 2, 5, and 15 min, respectively, during the IVGTT. During the clamp protocol, PI3-kinase was elevated by 5.3 +/- 1.3-, 8.0 +/- 2.6-, and 2.7 +/- 1.4-fold above basal at 15, 60, and 120 min, respectively. Insulin-stimulated PI3-kinase activity at 15 min post-insulin administration was significantly greater during the clamp protocol vs. the IVGTT (P < 0.05). These observations suggest that insulin-stimulated PI3-kinase activity is detectable in needle biopsies of human skeletal muscle, and furthermore, that the euglycemic, hyperinsulinemic clamp protocol may be a useful tool to assess insulin signaling in vivo.