Automatic Milking Systems in the Production of Parmigiano Reggiano Cheese: Effects on the Milk Quality and on Cheese Characteristics

The adoption of innovative processes, such as the automatic milking system (AMS), in the production of typical PDO cheeses, such as Parmigiano Reggiano, needs to be evaluated and tested, to verify its influence on milk quality and the typicality of the product. The present research was aimed to study the effect of the introduction of the AMS on the cheesemaking characteristics of the milk and the ripening process and the sensory properties of the Parmigiano Reggiano PDO cheese. Six cheesemaking trials were performed and, in each trial, two different separated pools of milk were submitted to the cheesemaking process in parallel, one from AMS and the other from a traditional milking parlor (TMP). AMS milk, in comparison with TMP one, showed higher content of lactose and calcium and lower contents of somatic cells, thermophilic lactic acid bacteria and chloride. Nevertheless, these changes were too small to influence the efficiency of the cheesemaking process and the cheese composition and its sensory profile. Moreover, cheeses made with AMS milk fully complied with the sensory characteristics of Parmigiano Reggiano cheese PDO, as defined by the PDO rules

Binge Eating Among Older Women: Prevalence Rates and Health Correlates Across Three Independent Samples

Background: Emerging research indicates that binge eating (BE; consuming unusually large amounts of food in one siting while feeling a loss of control) is prevalent among older women. Yet, health correlates of BE in older adult populations are poorly understood. The original study aimed to investigate BE prevalence, frequency, and health correlates in a sample of older adult women. Based on results from this first study, we then sought to replicate findings in two additional samples of older adult women from separate studies. Method: Using self-reported frequencies of BE from three separate samples of older women with very different demographics, we compared BE prevalence, frequency, and health correlates among older women. Study 1 (N=185) includes data collected online (86% White; 59% overweight/obese status). Study 2 (N=64) was conducted in person at a local food pantry (65% Hispanic; 47% household income\u3c$10,000/year). Study 3 (N=100) comprises data collected online (72% White; 50% Masters/Doctoral Degree). Results: Per DSM-5 frequency criterion of BE at least weekly, we found prevalence rates ranging from 19 to 26% across the three samples. Correlates of BE frequency included elevated negative mood, worry, BMI, and less nutritious food consumption. Conclusions: Across three very different samples in terms of race/ethnicity, education, food security status, measurements, and sampling methodology, we found fairly consistent rates of self-reported BE at least weekly (19–26%). Results suggest that BE is related to negative health indices among older women and support the need for more research in this populatio

Hepatic insulin resistance and altered gluconeogenic pathway in premature baboons

Premature infants have altered glucose regulation early in life and increased risk for diabetes in adulthood. Although prematurity leads to an increased risk of diabetes and metabolic syndrome in adult life, the role of hepatic glucose regulation and adaptation to an early extrauterine environment in preterm infants remain unknown. The purpose of this study was to investigate developmental differences in glucose metabolism, hepatic protein content, and gene expression of key insulin-signaling/gluconeogenic molecules. Fetal baboons were delivered at 67%, 75%, and term gestational age and euthanized at birth. Neonatal baboons were delivered prematurely (67% gestation), survived for two weeks, and compared with similar postnatal term animals and underwent serial hyperinsulinemic-euglycemic clamp studies. Premature baboons had decreased endogenous glucose production (EGP) compared with term animals. Consistent with these results, the gluconeogenic molecule, phosphoenolpyruvate carboxykinase messenger RNA, was decreased in preterm baboons compared with terms. Hepatic insulin signaling was altered by preterm birth as evidenced by decreased insulin receptor-b, p85 subunit of phosphoinositide 3-kinase, phosphorylated insulin receptor substrate 1, and Akt-1 under insulin-stimulated conditions. Furthermore, preterm baboons failed to have the normal increase in glycogen synthase kinase-a from fetal to postnatal life. The blunted responses in hepatic insulin signaling may contribute to the hyperglycemia of prematurity, while impaired EGP leads to hypoglycemia of prematurity

Effect of exenatide on splanchnic and peripheral glucose metabolism in type 2 diabetic subjects

OBJECTIVE: Our objective was to examine the mechanisms via which exenatide attenuates postprandial hyperglycemia in type 2 diabetes mellitus (T2DM). STUDY DESIGN: Seventeen T2DM patients (44 yr; seven females, 10 males; body mass index = 33.6 kg/m(2); glycosylated hemoglobin = 7.9%) received a mixed meal followed for 6 h with double-tracer technique ([1-(14)C]glucose orally; [3-(3)H]glucose i.v.) before and after 2 wk of exenatide. In protocol II (n = 5), but not in protocol I (n = 12), exenatide was given in the morning of the repeat meal. Total and oral glucose appearance rates (RaT and RaO, respectively), endogenous glucose production (EGP), splanchnic glucose uptake (75 g - RaO), and hepatic insulin resistance (basal EGP x fasting plasma insulin) were determined. RESULTS: After 2 wk of exenatide (protocol I), fasting plasma glucose decreased (from 10.2 to 7.6 mm) and mean postmeal plasma glucose decreased (from 13.2 to 11.3 mm) (P < 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.9 to 10.8 mumol/kg . min, P < 0.05), and hepatic insulin resistance declined (both P < 0.05). RaO, gastric emptying (acetaminophen area under the curve), and splanchnic glucose uptake did not change. In protocol II (exenatide given before repeat meal), fasting plasma glucose decreased (from 11.1 to 8.9 mm) and mean postmeal plasma glucose decreased (from 14.2 to 10.1 mm) (P < 0.05); fasting and meal-stimulated plasma insulin and glucagon did not change significantly. After exenatide, basal EGP decreased (from 13.4 to 10.7 mumol/kg . min, P = 0.05). RaT and RaO decreased markedly from 0-180 min after meal ingestion, consistent with exenatide\u27s action to delay gastric emptying. CONCLUSIONS: Exenatide improves 1) fasting hyperglycemia by reducing basal EGP and 2) postmeal hyperglycemia by reducing the appearance of oral glucose in the systemic circulation

Genetic disruption of sod1 gene causes glucose intolerance and impairs b-cell function

Oxidative stress has been associated with insulin resistance and type 2 diabetes. However, it is not clear whether oxidative damage is a cause or a consequence of the metabolic abnormalities present in diabetic subjects. The goal of this study was to determine whether inducing oxidative damage through genetic ablation of superoxide dismutase 1 (SOD1) leads to abnormalities in glucose homeostasis. We studied SOD1-null mice and wild-type (WT) littermates. Glucose tolerance was evaluated with intraperitoneal glucose tolerance tests. Peripheral and hepatic insulin sensitivity was quantitated with the euglycemic-hyperinsulinemic clamp. b-Cell function was determined with the hyperglycemic clamp and morphometric analysis of pancreatic islets. Genetic ablation of SOD1 caused glucose intolerance, which was associated with reduced in vivo b-cell insulin secretion and decreased b-cell volume. Peripheral and hepatic insulin sensitivity were not significantly altered in SOD1-null mice. High-fat diet caused glucose intolerance in WT mice but did not further worsen the glucose intolerance observed in standard chow-fed SOD1-null mice. Our findings suggest that oxidative stress per se does not play a major role in the pathogenesis of insulin resistance and demonstrate that oxidative stress caused by SOD1 ablation leads to glucose intolerance secondary to b-cell dysfunction. © 2013 by the American Diabetes Association

Metabolic effects of muraglitazar in type 2 diabetic subjects

AIM: To assess the effect of muraglitazar, a dual peroxisome proliferator-activated receptor (PPAR)gamma-alpha agonist, versus placebo on metabolic parameters and body composition in subjects with type 2 diabetes mellitus (T2DM). METHODS: Twenty-seven T2DM subjects received oral glucose tolerance test (OGTT), euglycaemic insulin clamp with deuterated glucose, measurement of total body fat (DEXA), quantitation of muscle/liver (MRS) and abdominal subcutaneous and visceral (MRI) fat, and then were randomized to receive, in addition to diet, muraglitazar (MURA), 5 mg/day, or placebo (PLAC) for 4 months. RESULTS: HbA1c(c) decreased similarly (2.1%) during both MURA and PLAC treatments despite significant weight gain with MURA (+2.5 kg) and weight loss with PLAC (-0.7 kg). Plasma triglyceride, LDL cholesterol, free fatty acid (FFA), hsCRP levels all decreased with MURA while plasma adiponectin and HDL cholesterol increased (p < 0.05-0.001). Total body (muscle), hepatic and adipose tissue sensitivity to insulin and beta cell function all improved with MURA (p < 0.05-0.01). Intramyocellular, hepatic and abdominal visceral fat content decreased, while total body and subcutaneous abdominal fat increased with MURA (p < 0.05-0.01). CONCLUSIONS: Muraglitazar (i) improves glycaemic control by enhancing insulin sensitivity and beta cell function in T2DM subjects, (ii) improves multiple cardiovascular risk factors, (iii) reduces muscle, visceral and hepatic fat content in T2DM subjects. Despite similar reduction in A1c with PLAC/diet, insulin sensitivity and beta cell function did not improve significantly

Metabolic syndrome predicts worse perioperative outcomes in patients treated with partial nephrectomy for renal cell carcinoma

OBJECTIVE: To test the association between metabolic syndrome (MetS) and its components (high blood pressure, body mass index [BMI] 65 30, altered fasting glucose, low high-density lipoprotein cholesterol and high triglycerides) on perioperative outcomes after partial nephrectomy (PN). METHODS: Within the National Inpatient Sample database (2000-2015) we identified all PN patients. First, temporal trends of MetS were reported. Second, the effect of MetS components was tested in multivariable logistic regression models predicting overall and specific perioperative complications. Third, we tested for dose-response from the concomitant effect of multiple MetS components. All models were weighted and adjusted for clustering, as well as all available patient and hospital characteristics. RESULTS: Of 25,875 patients: (1) 59.3% had high blood pressure, (2) 14.7% had BMI 65 30, (3) 21.7% had altered fasting glucose, (4) 20.2% had high triglycerides, and (5) &lt;0.01% had low high-density lipoprotein cholesterol. One vs 2 vs 3 vs 4 MetS components were recorded in 34.9% vs 22.9% vs 8.9% vs 2.2% patients. Of all, 11.1% exhibited 65 3 components and qualified for MetS. The rates of MetS increased over time (estimated annual percentage changes: +12.0%;P &lt;.001). The 4 tested MetS components (high blood pressure, BMI 65 30, altered fasting glucose, and high triglycerides) achieved independent predictor status in multivariable models predicting overall, cardiac, miscellaneous medical, vascular, and respiratory complications, as well as transfusions. Moreover, a statistically significant dose-response was confirmed for the same endpoints. CONCLUSION: MetS and its components consistently and strongly predict perioperative complications after PN. Moreover, the strength of the effect was directly proportional to the number of MetS components exhibited by each individual patient, even if formal MetS diagnosis of 65 3 components has not been m

Elevated Toll-Like Receptor 4 Expression and Signaling in Muscle From Insulin-Resistant Subjects

OBJECTIVE— Tall-like receptor (TLR)4 has been implicated in the pathogenesis of free fatty acid (FFA)-induced insulin resistance by activating inflammatory pathways, including inhibitor of κB (IκB)/nuclear factor κB (NFκB). However, it is not known whether insulin-resistant subjects have abnormal TLR4 signaling. We examined whether insulin-resistant subjects have abnormal TLR4 expression and TLR4-driven (IκB/NFκB) signaling in skeletal muscle