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Oral carotenoids and polyphenols have been suggested to induce photo-protective effects. The aim of the study was to test whether the combination of carotenoids and polyphenols produce greater protective effects from UV-induced damage to skin cells. Such damage is characterized by inflammation and oxidative stress; thus, the photo-protective effect can be partially explained by modulating the nuclear factor kappa B (NFκB) and antioxidant response element/Nrf2 (ARE/Nrf2) transcription systems, known as important regulators of these two processes. Indeed, it was found in keratinocytes that carotenoids and polyphenols inhibit UVB-induced NFκB activity and release of cytokine IL-6. A combination of tomato extract with rosemary extract inhibited UVB-induced release of IL-6 more than each of the compounds alone. Moreover, this combination synergistically activated ARE/Nrf2 transcription systems. Inflammatory cytokines such as IL-6 and TNFα induce the expression of matrix metalloproteinases (MMPs), which leads to collagen breakdown; thus, it is important to note that carnosic acid reduced TNFα-induced MMP-1 secretion from human dermal fibroblasts. The in vitro results suggest beneficial effects of phytonutrient combinations on skin health. To assure that clinical experiments to prove such effects in humans are feasible, the human bioavailability of carotenoids from tomato extract was tested, and nearly a twofold increase in their plasma concentrations was detected. This study demonstrates that carotenoids and polyphenols cooperate in balancing UV-induced skin cell damage, and suggests that NFκB and ARE/Nrf2 are involved in these effects.

The inflammasome has been recently implicated in obesity-associated dys-metabolism. However, of its products, the specific role of IL-1β was clinically demonstrated to mediate only the pancreatic beta-cell demise, and in mice mainly the intra-hepatic manifestations of obesity. Yet, it remains largely unknown if IL-1β, a cytokine believed to mainly function locally, could regulate dysfunctional inter-organ crosstalk in obesity. Here we show that High-fat-fed (HFF) mice exhibited a preferential increase of IL-1β in portal compared to systemic blood. Moreover, portally-drained mesenteric fat transplantation from IL-1βKO donors resulted in lower pyruvate-glucose flux compared to mice receiving wild-type (WT) transplant. These results raised a putative endocrine function for visceral fat-derived IL-1β in regulating hepatic gluconeogenic flux. IL-1βKO mice on HFF exhibited only a minor or no increase in adipose expression of pro-inflammatory genes (including macrophage M1 markers), Mac2-positive crown-like structures and CD11b-F4/80-double-positive macrophages, all of which were markedly increased in WT-HFF mice. Further consistent with autocrine/paracrine functions of IL-1β within adipose tissue, adipose tissue macrophage lipid content was increased in WT-HFF mice, but significantly less in IL-1βKO mice. Ex-vivo, adipose explants co-cultured with primary hepatocytes from WT or IL-1-receptor (IL-1RI)-KO mice suggested only a minor direct effect of adipose-derived IL-1β on hepatocyte insulin resistance. Importantly, although IL-1βKOs gained weight similarly to WT-HFF, they had larger fat depots with similar degree of adipocyte hypertrophy. Furthermore, adipogenesis genes and markers (pparg, cepba, fabp4, glut4) that were decreased by HFF in WT, were paradoxically elevated in IL-1βKO-HFF mice. These local alterations in adipose tissue inflammation and expansion correlated with a lower liver size, less hepatic steatosis, and preserved insulin sensitivity. Collectively, we demonstrate that by promoting adipose inflammation and limiting fat tissue expandability, IL-1β supports ectopic fat accumulation in hepatocytes and adipose-tissue macrophages, contributing to impaired fat-liver crosstalk in nutritional obesity.

The inflammasome has been recently implicated in obesity-associated dys-metabolism. However, of its products, the specific role of IL-1[beta] was clinically demonstrated to mediate only the pancreatic beta-cell demise, and in mice mainly the intra-hepatic manifestations of obesity. Yet, it remains largely unknown if IL-1[beta], a cytokine believed to mainly function locally, could regulate dysfunctional inter-organ crosstalk in obesity. Here we show that High-fat-fed (HFF) mice exhibited a preferential increase of IL-1[beta] in portal compared to systemic blood. Moreover, portally-drained mesenteric fat transplantation from IL-1[beta]KO donors resulted in lower pyruvate-glucose flux compared to mice receiving wild-type (WT) transplant. These results raised a putative endocrine function for visceral fat-derived IL-1[beta] in regulating hepatic gluconeogenic flux. IL-1[beta]KO mice on HFF exhibited only a minor or no increase in adipose expression of pro-inflammatory genes (including macrophage M1 markers), Mac2-positive crown-like structures and CD11b-F4/80-double-positive macrophages, all of which were markedly increased in WT-HFF mice. Further consistent with autocrine/paracrine functions of IL-1[beta] within adipose tissue, adipose tissue macrophage lipid content was increased in WT-HFF mice, but significantly less in IL-1[beta]KO mice. Ex-vivo, adipose explants co-cultured with primary hepatocytes from WT or IL-1-receptor (IL-1RI)-KO mice suggested only a minor direct effect of adipose-derived IL-1[beta] on hepatocyte insulin resistance. Importantly, although IL-1[beta]KOs gained weight similarly to WT-HFF, they had larger fat depots with similar degree of adipocyte hypertrophy. Furthermore, adipogenesis genes and markers (pparg, cepba, fabp4, glut4) that were decreased by HFF in WT, were paradoxically elevated in IL-1[beta]KO-HFF mice. These local alterations in adipose tissue inflammation and expansion correlated with a lower liver size, less hepatic steatosis, and preserved insulin sensitivity. Collectively, we demonstrate that by promoting adipose inflammation and limiting fat tissue expandability, IL-1[beta] supports ectopic fat accumulation in hepatocytes and adipose-tissue macrophages, contributing to impaired fat-liver crosstalk in nutritional obesity.

The transcription factor CCA1 (CIRCADIAN CLOCK ASSOCIATED 1) participates in both light and circadian clock regulation in Arabidopsis. Two sets of transgenic plants in which GFP was fused to the CCA1 promoter with (1.3-kb fragment) or without (1.01-kb fragment) its 5'UTR were engineered. The transgenic plants transformed with the promoter including the 5'UTR had altered circadian regulation resulting in elongated hypocotyls, a bushy appearance and delayed flowering. In contrast, the transgenic plants transformed with the promoter without the 5'UTR showed earlier flowering than the wild type. Changes in CCA1, LHY and TOC1 gene expression were investigated under light-dark (L:D) fluctuations, continuous darkness (D:D) and continuous light (L:L). The circadian expression of CCA1 was altered in both sets of transgenic plants, being repressed in the plants transformed with the 1.01-kb fragment and constitutively overexpressed in those transformed with the 1.3-kb fragment. Under L:D conditions, regulation of LHY and TOC1 expression was separated from CCA1 regulation in both sets of transgenic plants, with intact rhythmic expression of both LHY and TOC1. Under D:D conditions, the rhythmic expression of LHY and TOC1 was lost in the 1.3 plants but retained with some erratic pattern under L:L conditions. In the 1.01 plants, under both D:D and L:L conditions the rhythmic expression was retained. These results indicate separate light-induced signal-transmission pathways for LHY and CCA1.

The transcription factor CCA1 (CIRCADIAN CLOCK ASSOCIATED 1) participates in both light and circadian clock regulation in Arabidopsis. Two sets of transgenic plants in which GFP was fused to the CCA1 promoter with (1.3-kb fragment) or without (1.01-kb fragment) its 5′UTR were engineered. The transgenic plants transformed with the promoter including the 5′UTR had altered circadian regulation resulting in elongated hypocotyls, a bushy appearance and delayed flowering. In contrast, the transgenic plants transformed with the promoter without the 5′UTR showed earlier flowering than the wild type. Changes in CCA1, LHY and TOC1 gene expression were investigated under light-dark (L:D) fluctuations, continuous darkness (D:D) and continuous light (L:L). The circadian expression of CCA1 was altered in both sets of transgenic plants, being repressed in the plants transformed with the 1.01-kb fragment and constitutively overexpressed in those transformed with the 1.3-kb fragment. Under L:D conditions, regulation of LHY and TOC1 expression was separated from CCA1 regulation in both sets of transgenic plants, with intact rhythmic expression of both LHY and TOC1. Under D:D conditions, the rhythmic expression of LHY and TOC1 was lost in the 1.3 plants but retained with some erratic pattern under L:L conditions. In the 1.01 plants, under both D:D and L:L conditions the rhythmic expression was retained. These results indicate separate light-induced signal-transmission pathways for LHY and CCA1.