Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose-or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults. IntroductionStudies investigating the effects of fructose consumption in humans and animals have been comprehensively reviewed (1-4), and while strong evidence exists that consumption of diets high in fructose results in increased de novo lipogenesis (DNL), dyslipidemia, insulin resistance, and obesity in animals, direct experimental evidence that consumption of fructose promotes DNL, dyslipidemia, insulin resistance, glucose intolerance, and obesity in humans is lacking. Thus, we have investigated and compared the biological effects of the 2 major simple sugars in the diet, glucose and fructose, on BW and regional fat deposition and on indices of lipid and carbohydrate metabolism in older, overweight and obese men and women.We sought to answer the following questions: (a) Does consumption of fructose with an ad libitum diet promote greater BW gain and have differential effects on regional adipose deposition and adipose gene expression compared with consumption of glucose with an ad libitum diet? (b) Does consumption of fructose induce dyslipidemia compared with consumption of glucose? (c) Is fructose-induced hypertriglyceridemia the result of increased rates

BackgroundSevere illness due to 2009 pandemic A(H1N1) infection has been reported among persons who are obese or morbidly obese. We assessed whether obesity is a risk factor for hospitalization and death due to 2009 pandemic influenza A(H1N1), independent of chronic medical conditions considered by the Advisory Committee on Immunization Practices (ACIP) to increase the risk of influenza-related complications.Methodology/Principal FindingsWe used a case-cohort design to compare cases of hospitalizations and deaths from 2009 pandemic A(H1N1) influenza occurring between April–July, 2009, with a cohort of the U.S. population estimated from the 2003–2006 National Health and Nutrition Examination Survey (NHANES); pregnant women and children <2 years old were excluded. For hospitalizations, we defined categories of relative weight by body mass index (BMI, kg/m2); for deaths, obesity or morbid obesity was recorded on medical charts, and death certificates. Odds ratio (OR) of being in each BMI category was determined; normal weight was the reference category. Overall, 361 hospitalizations and 233 deaths included information to determine BMI category and presence of ACIP-recognized medical conditions. Among ≥20 year olds, hospitalization was associated with being morbidly obese (BMI≥40) for individuals with ACIP-recognized chronic conditions (OR = 4.9, 95% CI 2.4–9.9) and without ACIP-recognized chronic conditions (OR = 4.7, 95%CI 1.3–17.2). Among 2–19 year olds, hospitalization was associated with being underweight (BMI≤5th percentile) among those with (OR = 12.5, 95%CI 3.4–45.5) and without (OR = 5.5, 95%CI 1.3–22.5) ACIP-recognized chronic conditions. Death was not associated with BMI category among individuals 2–19 years old. Among individuals aged ≥20 years without ACIP-recognized chronic medical conditions death was associated with obesity (OR = 3.1, 95%CI: 1.5–6.6) and morbid obesity (OR = 7.6, 95%CI 2.1–27.9).Conclusions/SignificanceOur findings support observations that morbid obesity may be associated with hospitalization and possibly death due to 2009 pandemic H1N1 infection. These complications could be prevented by early antiviral therapy and vaccination.

For high temperature thermoelectric applications, Yb14MnSb11 has a maximum thermoelectric figure of merit (zT) of ∼1.0 at 1273 K. Such a high zT is found despite a carrier concentration that is higher than typical thermoelectric materials. Here, we reduce the carrier concentration with the discovery of a continuous transition between metallic Yb14MnSb11 and semiconducting Yb14AlSb11. Yb14Mn1‐xAlxSb11 forms a solid solution where the free carrier concentration gradually changes as expected from the Zintl valence formalism. Throughout this transition the electronic properties are found to obey a rigid band model with a band gap of 0.5 eV and an effective mass of 3 me. As the carrier concentration decreases, an increase in the Seebeck coefficient is observed at the expense of an increased electrical resistivity. At the optimum carrier concentration, a maximum zT of 1.3 at 1223 K is obtained, which is more than twice that of the state‐of‐the‐art Si0.8Ge0.2 flown by NASA.

Analyses of inflammation inducing Th cells revealed that a portion of these cells express both IFN‐γ and IL‐17, suggesting that Th1 and/or Th17 may switch their phenotype. Here, we examined phenotype retention in a system in which polarized Th1 or Th17 cells specific against hen egg lysozyme (HEL) induce ocular inflammation in recipient mice expressing HEL in their eyes. Whereas no switching to Th17 was detected in Th1 recipient eyes, substantial proportions of transferred Th17 expressed IFN‐γ, or both IFN‐γ and IL‐17 in Th17 recipient eyes. The phenotype switch of Th17 cells increased with time and was attributed to exposure to IL‐12 that is expressed in the inflamed eyes. Incubation in vitro with Th1 polarizing cocktail (IL‐2+IL‐12) converted most Th17 into IFN‐γ or IFN‐γ/IL‐17 expressing cells, but no reciprocal conversion was noted with Th1 cells. Furthermore, whereas Th1 cells did not express ROR‐γt following incubation with Th17 polarizing cocktail, Th17 expressed T‐bet following incubation with Th1 cocktail. Thus, polarized Th1 cells fully retain their phenotype, while Th17 switch and express IFN‐γ or both IFN‐γ and IL‐17, as well as T‐bet, following exposure to IL‐12. This study is supported by NEI/NIH intramural program.