Mean and total CVL provide markers of access to care and treatment, are indicators of the population's viral burden, and are useful in assessing trends in local HIV/AIDS epidemics. Measurement of CVL is a novel tool for assessing the potential impact of population-level HIV prevention and treatment interventions.
Fourteen mature, ovariectomized, western-range ewes with an initial mean BW of 72 +/- 4.5 kg and mean condition score (CS) of 7.5 +/- .3 were used to evaluate the relationship between CS and body composition. Diets of chopped straw and alfalfa hay were formulated to provide either maintenance energy or less than maintenance energy (100 or 60% of ME) to induce changes in BW and CS. After 180 d, ewes were weighted, scored for body condition, and slaughtered. All carcass components, viscera, and organs were analyzed for lipid, DM, and ash, and protein was determined by difference. Body weight and CS values were related by regression analysis to percentage of composition and weights of carcass components, carcass, and empty body. Body weight and CS were highly correlated (r = .89) and analysis indicated that each increase in CS resulted in an increase of 5.1 kg of BW. Condition score accounted for more variation of percentage of lipid in the empty body (R2 = .95) and carcass (R2 = .90) than did BW (R2 = .84 and .80, respectively). In contrast, BW accounted for more of the variation in carcass weight (R2 = .97) and empty BW (R2 = .99). Inclusion of both BW and CS in regression models did not increase the variation accounted for with the single best predictor. With mature western-range ewes in this study, CS was highly related to carcass lipids and could be used to describe energy reserves available to ewes.
Inflammation plays a role in trans-10, cis-12 (10,12)-conjugated linoleic acid (CLA)-mediated delipidation and insulin resistance in adipocytes. Given the anti-inflammatory role of resveratrol (RSV), we hypothesized that RSV would attenuate inflammation and insulin resistance caused by 10,12 CLA in human adipocytes. RSV blocked 10,12 CLA induction of the inflammatory response by preventing activation of extracellular signal-related kinase and induction of inflammatory gene expression (i.e., IL-6, IL-8, IL-1b) within 12 h. Similarly, RSV suppressed 10,12 CLA-mediated activation of the inflammatory prostaglandin pathway involving phospholipase A 2 , cyclooxygenase-2, and PGF 2a . In addition, RSV attenuated 10,12 CLA increase of intracellular calcium and reactive oxygen species associated with cellular stress, and activation of stress-related proteins (i.e., activating transcription factor 3, JNK) within 12 h. 10,12 CLA-mediated insulin resistance and suppression of fatty acid uptake and triglyceride content were attenuated by RSV. Finally, 10,12 CLA-mediated decrease of peroxisome proliferator-activated receptor g (PPARg) protein levels and activation of a peroxisome proliferator response element (PPRE) reporter were prevented by RSV. RSV increased the basal activity of PPRE, suggesting that RSV increases PPARg activity. Collectively, these data demonstrate for the first time that RSV prevents 10,12 CLAmediated insulin resistance and delipidation in human adipocytes by attenuating inflammation and cellular stress and increasing PPARg activity. Feeding a mixture of conjugated linoleic acid (CLA) isomers [i.e., trans-10, cis-12 (10,12) CLA and cis-9, trans-11 (9,11) CLA] reduces adiposity in animals (1) and some humans (2). The triglyceride (TG)-lowering properties of CLA appear to be due exclusively to the 10,12 isomer (3-5), and involve decreased uptake and metabolism of glucose and fatty acids (FA)s (6), and increased lipolysis (7) in adipocytes. These anti-obesity properties of 10,12 CLA are dependent on the activation of mitogen-activated protein kinase kinase/extracellular signal-related kinase (MEK/ERK) (6) and nuclear factor kB (NFkB) (8, 9) in adipocytes. These signaling pathways induced by 10,12 CLA are linked to the induction and secretion of cytokines (8, 9), which are known to antagonize peroxisome proliferator-activated receptor g (PPARg) target gene expression and insulin sensitivity (10-15). Consistent with these data, 10,12 CLA supplementation of humans is associated with hyperglycemia, insulin resistance, elevated levels of inflammatory prostaglandins (PGs) and cytokines, and dyslipidemia (16)(17)(18).Recently, supplementation of mice and 3T3-L1 adipocytes with 10,12 CLA has been shown to activate the integrated stress response (ISR) pathway (19), which is linked to inflammation, insulin resistance, and endoplasmic reticulum (ER) stress (20). Cellular stress can be caused by a relatively disproportional influx of macronutrients that adversely affect organelle function, including the mitoc...
Background: Obesity-associated inflammation is characterized by an increased abundance of macrophages (MFs) in white adipose tissue (WAT), leading to the production of inflammatory cytokines, chemokines and prostaglandins (PGs) that can cause insulin resistance. Grape powder extract (GPE) is rich in phenolic phytochemicals that possess anti-oxidant and antiinflammatory properties. Objective: We examined the ability of GPE to prevent lipopolysaccharide (LPS)-mediated inflammation in human MFs and silence the cross-talk between human MFs and adipocytes. Design: We investigated the effect of GPE pretreatment on LPS-mediated activation of mitogen activated protein kinases (MAPKs), nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1), and induction of inflammatory genes in human MFs (that is, differentiated U937 cells). In addition, we determined the effect of GPE pretreatment of MFs on inflammation and insulin resistance in primary human adipocytes incubated with LPS-challenged MF-conditioned medium (MF-CM). Methods and Results: Pretreatment of MFs with GPE attenuated LPS-induction of inflammatory cytokines, such as tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6) and IL-1b; chemokines, such as IL-8 and interferon-g inducible protein-10 (IP-10); and a marker of PG production, cyclooxygenase-2 (COX-2). Grape powder extract also attenuated LPS activation of MAPKs, NF-kB and AP-1 (c-Jun), as evidenced by decreased (1) phosphorylation of c-Jun NH 2 -terminal kinase (JNK) and p38; (2) degradation of IkBa and activation of an NF-kB reporter construct; and (3) phosphorylation of c-Jun and Elk-1. Using LPSchallenged MF-CM, GPE pretreatment attenuated MF-mediated inflammatory gene expression, activation of an NF-kB reporter and suppression of insulin-stimulated glucose uptake in human adipocytes. Conclusion:Collectively, these data demonstrate that GPE attenuates LPS-mediated inflammation in MFs, possibly by decreasing the activation of MAPKs, NF-kB and AP-1, and that GPE decreases the capacity of LPS-stimulated MFs to inflame adipocytes and cause insulin resistance.
The xanthones, alpha- and gamma-mangostin (MG), are major bioactive compounds found in mangosteen and are reported to have antiinflammatory properties in several murine models. Given the association between obesity, chronic low-grade inflammation, and insulin resistance, we examined the effects of alpha- and gamma-MG on markers of inflammation and insulin resistance in primary cultures of newly differentiated human adipocytes treated with lipopolysaccharide (LPS). alpha- and gamma-MG decreased the induction by LPS of inflammatory genes, including tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, IL-8, monocyte chemoattractant protein-1, and Toll-like receptor-2. Moreover, alpha- and gamma-MG attenuated LPS activation of the mitogen-activated protein kinases (MAPK) c-jun NH(2)-terminal kinase, extracellular signal-related kinase, and p38. alpha- and gamma-MG also attenuated LPS activation of c-Jun and activator protein (AP)-1 activity. gamma-MG was more effective than alpha-MG on an equimolar basis. Furthermore, gamma-MG but not alpha-MG attenuated LPS-mediated IkappaB-alpha degradation and nuclear factor-kappaB (NF-kappaB) activity. In addition, gamma-MG prevented the suppression by LPS of insulin-stimulated glucose uptake and PPAR-gamma and adiponectin gene expression. Taken together, these data demonstrate that MG attenuates LPS-mediated inflammation and insulin resistance in human adipocytes, possibly by inhibiting the activation of MAPK, NF-kappaB, and AP-1.
The present study examines initial symptom presentation among participants, outcomes, and social validity for a group treatment for child sexual abuse delivered at a child advocacy center. Participants were 97 children and their nonoffending caregivers who were referred to Project SAFE (Sexual Abuse Family Education), a standardized, 12-week cognitive-behavioral group treatment for families who have experienced child sexual abuse. Sixty-four percent of children presented with clinically significant symptoms on at least one measure with established clinical cutoffs. Caregivers of children who presented with clinically significant symptoms reported more distress about their competence as caregivers. Children who presented as subclinical were more likely to have experienced intrafamilial sexual abuse. Posttreatment results indicated significant improvements in functioning for all children who participated in treatment, with greater improvements reported for children who initially presented with clinically significant symptoms. Overall, the program was rated favorably on the posttreatment evaluation of social validity.
We showed previously in cultures of primary human adipocytes and preadipocytes that lipopolysaccharide and trans-10,cis-12-conjugated linoleic acid (10,12-CLA) activate the inflammatory signaling that promotes insulin resistance. Because our published data demonstrated that preadipocytes are the primary instigators of inflammatory signaling in lipopolysaccharide-treated cultures, we hypothesized that they played the same role in 10,12-CLA-mediated inflammation. To test this hypothesis, we employed four distinct models. In model 1, a differentiation model, CLA activation of MAPK and induction of interleukin-8 (IL-8), IL-6, IL-1, and cyclo-oxygenase-2 (COX-2) were greatest in differentiated compared with undifferentiated cultures. In model 2, a cell separation model, the mRNA levels of these inflammatory proteins were increased by 10,12-CLA compared with bovine serum albumin vehicle in the adipocyte fraction and the preadipocyte fraction. In model 3, a co-culture insert model, inserts containing ϳ50% adipocytes (AD50) or ϳ100% preadipocytes (AD0) were suspended over wells containing AD50 or AD0 cultures. 10,12-CLA-induced IL-8, IL-6, IL-1, and COX-2 mRNA levels were highest in AD50 cultures when co-cultured with AD0 inserts. In model 4, a conditioned medium (CM) model, CM collected from CLAtreated AD50 but not AD0 cultures induced IL-8 and IL-6 mRNA levels and activated phosphorylation of MAPK in naive AD0 and AD50 cultures. Consistent with these data, 10,12-CLA-mediated secretions of IL-8 and IL-6 from AD50 cultures were higher than from AD0 cultures. Notably, blocking adipocytokine secretion prevented the inflammatory capacity of CM from 10,12-CLA-treated cultures. These data suggest that CLA instigates the release of inflammatory signals from adipocytes that subsequently activate adjacent preadipocytes.
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