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Coplanar polychlorinated biphenyls (PCBs) promote adipocyte inflammation and impair glucose homeostasis in lean mice. The diabetes-promoting effects of lipophilic PCBs have been observed only during weight loss in obese mice. The molecular mechanisms linking PCB exposures to impaired glucose metabolism are unclear. In this study we tested the hypothesis that coplanar PCBs act at adipocyte aryl hydrocarbon receptors (AhRs) to promote adipose inflammation and impair glucose homeostasis in lean mice and in obese mice during weight loss. PCB-77 administration impaired glucose and insulin tolerance in LF (low fat diet)-fed control (AhR(fl/fl)) mice but not in adipocyte AhR-deficient mice (AhR(AdQ)). Unexpectedly, AhR(AdQ) mice exhibited increased fat mass when fed a standard LF or high fat (HF) diet. In mice fed a HF diet, both genotypes became obese, but AhR(AdQ) mice administered vehicle (VEH) exhibited increased body weight, adipose mass, adipose inflammation, and impaired glucose tolerance compared with AhR(fl/fl) controls. Impairment of glucose homeostasis in response to PCB-77 was not observed in obese mice of either genotype. However, upon weight loss, AhR(fl/fl) mice administered PCB-77 exhibited increased abundance of adipose tumor necrosis factor-α (TNF-α) mRNA and impaired glucose homeostasis compared with those administered VEH. In contrast, PCB-77 had no effect on TNF-α or glucose homeostasis in AhR(AdQ) mice exhibiting weight loss. Our results demonstrate that adipocyte AhR mediates PCB-induced adipose inflammation and impairment of glucose homeostasis in mice. Moreover, deficiency of AhR in adipocytes augmented the development of obesity, indicating that endogenous ligand(s) for AhR regulate adipose homeostasis.

Angiotensin II (AngII) facilitates sympathetic neurotransmission by regulating norepinephrine (NE) synthesis, release, and uptake. These effects of AngII contribute to cardiovascular control. Previous studies in our laboratory demonstrated that chronic AngII infusion decreased body weight of rats. We hypothesized that AngII facilitates sympathetic neurotransmission to adipose tissue and may thereby decrease body weight. The effect of chronic AngII infusion on the NE uptake transporter and NE turnover was examined in metabolic (interscapular brown adipose tissue, ISBAT; epididymal fat, EF) and cardiovascular tissues (left ventricle, LV; kidney) of rats. To examine the uptake transporter saturation isotherms were performed using [3H]nisoxetine (NIS). At doses that lowered body weight, AngII significantly increased ISBAT [3H]NIS binding density. To quantify NE turnover, alpha‐methyl‐para‐tyrosine (AMPT) was injected in saline‐infused, AngII‐infused, or saline‐infused rats that were pair‐fed to food intake of AngII‐infused rats. AngII significantly increased the rate of NE decline in all tissues compared to saline. The rate of NE decline in EF was increased to a similar extent by AngII and by pair feeding. In rats administered AngII and propranolol, reductions in food and water intake and body weight were eliminated. These data support the hypothesis that AngII facilitates sympathetic neurotransmission to adipose tissue. Increased sympathetic neurotransmission to adipose tissue following AngII exposure is suggested to contribute to reductions in body weight. e00014 We demonstrate that infusion doses of angiotensin II in rats that lower body weight result in an increase in levels of the norepinephrine uptake transporter and elevated catcholamine turnover in adipose tissue. Angiotensin II‐induced regulation of body weight was abolished by the beta‐adrenergic receptor antagonist, propranolol. Heightened activity of the renin–angiotensin system in certain disease states not only regulates the cardiovascular system, but also may regulate body weight.

Previous studies demonstrated that coplanar polychlorinated biphenyls (PCBs) promote proinflammatory gene expression in adipocytes. PCBs are highly lipophilic and accumulate in adipose tissue, a site of insulin resistance in persons with type 2 diabetes. We investigated the in vitro and in vivo effects of coplanar PCBs on adipose expression of tumor necrosis factor α (TNF-α) and on glucose and insulin homeostasis in lean and obese mice. We quantified glucose and insulin tolerance, as well as TNF-α levels, in liver, muscle, and adipose tissue of male C57BL/6 mice administered vehicle, PCB-77, or PCB-126 and fed a low fat (LF) diet. Another group of mice administered vehicle or PCB-77 were fed a high fat (HF) diet for 12 weeks; the diet was then switched from HF to LF for 4 weeks to induce weight loss. We quantified glucose and insulin tolerance and adipose TNF-α expression in these mice. In addition, we used in vitro and in vivo studies to quantify aryl hydrocarbon receptor (AhR)-dependent effects of PCB-77 on parameters of glucose homeostasis. Treatment with coplanar PCBs resulted in sustained impairment of glucose and insulin tolerance in mice fed the LF diet. In PCB-77-treated mice, TNF-α expression was increased in adipose tissue but not in liver or muscle. PCB-77 levels were strikingly higher in adipose tissue than in liver or serum. Antagonism of AhR abolished both in vitro and in vivo effects of PCB-77. In obese mice, PCB-77 had no effect on glucose homeostasis, but glucose homeostasis was impaired after weight loss. Coplanar PCBs impaired glucose homeostasis in lean mice and in obese mice following weight loss. Adipose-specific elevations in TNF-α expression by PCBs may contribute to impaired glucose homeostasis.

Lipophilic polychlorinated biphenyls (PCBs) accumulate with obesity, but during weight loss, liberated PCBs act as ligands of the aryl hydrocarbon receptor (AhR) to negatively influence health. Previous studies demonstrated that PCB-77 administration to obese male mice impaired glucose tolerance during weight loss. Recent studies indicate higher toxic equivalencies of dioxin-like PCBs in exposed females than males. We compared effects of PCB-77 on weight gain or loss and glucose homeostasis in male vs. female mice. We defined effects of AhR deficiency during weight gain or loss in male and female mice exposed to PCB-77. Study design was vehicle (VEH) or PCB-77 administration while fed a high-fat (HF) diet for 12 wk, followed by weight loss for 4 wk. The following groups were examined: male and female C57BL/6 mice administered VEH or PCB-77, female [Formula: see text] and [Formula: see text] mice administered VEH or PCB-77, and male [Formula: see text] and [Formula: see text] mice administered PCB-77. Glucose tolerance was quantified during weight gain (week 11) and loss (week 15); liver and adipose AhR and IRS2 (insulin receptor substrate 2) mRNA abundance, and PCB-77 concentrations were quantified at week 16. PCB-77 attenuated development of obesity in females but not males. During weight loss, PCB-77 impaired glucose tolerance of males. AhR-deficient females (VEH) were resistant to diet-induced obesity. Compared with VEH-treated mice, HF-fed [Formula: see text] females treated with PCB-77 has less weight gain, and [Formula: see text] females had greater weight gain. During weight loss, [Formula: see text] females but not [Formula: see text] males treated with PCB-77 exhibited impaired glucose tolerance. In [Formula: see text] females administered PCB-77, IRS2 mRNA abundance was lower in adipose tissue compared with VEH-treated mice. Male and female mice responded differently to PCB-77 and AhR deficiency in body weight (BW) regulation and glucose homeostasis. AhR deficiency reversed PCB-77-induced glucose impairment of obese males losing weight but augmented glucose intolerance of females. These results demonstrate sex differences in PCB-77-induced regulation of glucose homeostasis of mice. https://doi.org/10.1289/EHP4133.

Practical help is on the way for UK doctors who are facing a rising number of claims for clinical negligence. Major reform in the UK is discussed.

Adipocytes express renin-angiotensin system (RAS) components, including angiotensinogen (Agt), the precursor to angiotensin II (AngII), and the angiotensin type 1a receptor (AT1aR). The RAS contributes to atherosclerosis, and AngII infusion causes abdominal aortic aneurysm (AAA) formation. Obesity, an established vascular risk factor, exhibits a dysregulated RAS. We studied effects of adipocyte Agt or AT1aR deficiency on diet-induced atherosclerosis and AngII-induced AAAs in male low density lipoprotein receptor (Ldlr) deficient mice. For atherosclerosis, male control or adipocyte Agt/AT1aR deficient mice were fed Western diet for 3 months. There was no effect of adipocyte Agt or AT1aR deficiency on body weight, serum cholesterol concentrations, or atherosclerotic lesions. For AngII-induced AAAs, male control and adipocyte Agt/AT1aR deficient Ldlr-/- mice fed Western diet were infused with AngII. Adipocyte Agt deficiency had no effect on body weight, serum cholesterol concentrations, abdominal aortic lumen diameter, AAA incidence, or atherosclerosis. Control, but not adipocyte AT1aR deficient mice lost weight during AngII infusion. The size of adipocytes in white fat was increased in adipocyte AT1aR deficient mice with no significant influences on abdominal aortic lumen diameter, AAA incidence, or atherosclerosis. To define mechanisms, male Ldlr-/- mice were fed standard or Western diet (1 or 3 months) and Agt or AT1aR mRNA abundance quantified in periaortic fat (PAF). Agt mRNA abundance in abdominal PAF increased over time in both diet groups, with modest diet-induced reductions in thoracic PAF Agt mRNA abundance. There was an effect of diet duration on AT1aR mRNA abundance in thoracic PAF, and an interaction between diet and time on abdominal PAF AT1aR mRNA abundance. In conclusion, adipocyte Agt or AT1aR deficiency had minimal effects on atherosclerosis or AngII-induced AAAs. However, adipocyte AT1aR deficient mice exhibited increased adipocyte size. Diet-induced regulation of Agt or AT1aR mRNA abundance in PAF may have contributed to these findings.

Published to mark the Civil War sesquicentennial, The Yellowhammer War collects new essays on Alabama’s role in, and experience of, the bloody national conflict and its aftermath. During the first winter of the war, Confederate soldiers derided the men of an Alabama Confederate unit for their yellow-trimmed uniforms that allegedly resembled the plumage of the yellow-shafted flicker or “yellowhammer” (now the Northern Flicker, Colaptes auratus , and the state bird of Alabama). The soldiers’ nickname, “Yellowhammers,” came from this epithet. After the war, Alabama veterans proudly wore yellowhammer feathers in their hats or lapels when attending reunions. Celebrations throughout the state have often expanded on that pageantry and glorified the figures, events, and battles of the Civil War with sometimes dubious attention to historical fact and little awareness of those who supported, resisted, or tolerated the war off the battlefield. Many books about Alabama’s role in the Civil War have focused serious attention on the military and political history of the war. The Yellowhammer War likewise examines the military and political history of Alabama’s Civil War contributions, but it also covers areas of study usually neglected by centennial scholars, such as race, women, the home front, and Reconstruction. From Patricia A. Hoskins’s look at Jews in Alabama during the Civil War and Jennifer Ann Newman Treviño’s examination of white women’s attitudes during secession to Harriet E. Amos Doss’s study of the reaction of Alabamians to Lincoln’s Assassination and Jason J. Battles’s essay on the Freedman’s Bureau, readers are treated to a broader canvas of topics on the Civil War and the state. CONTRIBUTORS Jason J. Battles / Lonnie A. Burnett / Harriet E. Amos Doss / Bertis English / Michael W. Fitzgerald / Jennifer Lynn Gross / Patricia A. Hoskins / Kenneth W. Noe / Victoria E. Ott  / Terry L. Seip / Ben H. Severance / Kristopher A. Teters / Jennifer Ann Newman Treviño / Sarah Woolfolk Wiggins / Brian Steel Wills Published in Cooperation with the Frances S. Summersell Center for the Study of the South

EINDOVEN, the Netherlands--Unlike profits, in novation and imagination have never been in short supply at N.V. Philips Gloeilampenfabrieken. Nearly a century ago, the Dutch multinational manufactured one of Europe's first...

LONDON - Britain`s recession is starting to alarm economists, who fear the government-induced slowdown to quash inflation may become one of the worst slumps in decades. \"We see a deep and prolonged recession. In terms of cumulative gross domestic product loss, it could be the second-worst recession since the Second World War,\" said Peter Spencer, an economist at stockbrokers Shearson Lehman. Economists are increasingly questioning the government`s claim that the recession will be modest.