Effetto della restrizione alimentare di dieci ore al giorno su peso corporeo, pressione arteriosa e lipidi aterogeni in pazienti affetti da sindrome metabolica

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The Social Aspects of Sexual Health: A Twitter-Based Analysis of Valentine’s Day Perception

Sentiment analysis (SA) is a technique aimed at extracting opinions and sentiments through the analysis of text, often used in healthcare research to understand patients’ needs and interests. Data from social networks, such as Twitter, can provide useful insights on sexual behavior. We aimed to assess the perception of Valentine’s Day by performing SA on tweets we collected between 28 January and 13 February 2019. Analysis was done using ad hoc software. A total of 883,615 unique tweets containing the word “valentine” in their text were collected. Geo-localization was available for 48,918 tweets; most the tweets came from the US (36,889, 75.41%), the UK (2605, 5.33%) and Canada (1661, 3.4%). The number of tweets increased approaching February 14. “Love” was the most recurring word, appearing in 111,981 tweets, followed by “gift” (55,136), “special” (34,518) and “happy” (33,913). Overall, 7318 tweets mentioned “sex”: among these tweets, the most recurring words were “sexy” (2317 tweets), “love” (1394) and “gift” (679); words pertaining to intimacy and sexual activity, such as “lingerie”, “porn”, and “date” were less common. In conclusion, tweets about Valentine’s Day mostly focus on the emotions, or on the material aspect of the celebration, and the sexual aspect of Valentine’s Day is rarely mentioned

Male Sexual Health and Sexual Behaviors during the First National COVID-19 Lockdown in a Western Country: A Real-Life, Web-Based Study

Restriction measures enacted during the COVID-19 pandemic had severe effects on male sexual and reproductive health. We aimed to investigate the real-life impact and perception of sexual function in 2020 in Italy, as the first Western country experiencing a national lockdown by measuring relative search volume for keywords pertaining to sexual health and behaviors provided by Google Trends and sales data for pro-erectile treatments. No significant change was observed for erectile dysfunction and premature ejaculation. Interest towards most phosphodiesterase type 5 inhibitors decreased significantly during lockdown (e.g., sildenafil, p = 0.0002; tadalafil p = 0.0016), then reverted to pre-lockdown levels (e.g., sildenafil, p p p = 0.0292). A subsequent recovery to previous levels at the end of the social confinement was also found (e.g., after vs. before lockdown, sildenafil, p = 0.8459; tadalafil p = 0.1166). During lockdown, interest towards pornography significantly increased during restrictions (p = 0.0053) and remained high (after vs. before lockdown, p = 0.0004), whereas interest towards paid and casual sex declined (p = 0.0015 and p = 0.049, respectively), then reverted to previous levels (after vs. before lockdown, p = 0.3969 and 0.8373, respectively). During the first Italian lockdown, we observed a transient but measurable decrease of sexual health-seeking behaviors and changes in sexual behaviors, with unknown impact for sexual medicine and public health

Gut: A key player in the pathogenesis of type 2 diabetes?

The gut regulates glucose and energy homeostasis; thus, the presence of ingested nutrients into the gut activates sensing mechanisms that affect both glucose homeostasis and regulate food intake. Increasing evidence suggest that gut may also play a key role in the pathogenesis of type 2 diabetes which may be related to both the intestinal microbiological profile and patterns of gut hormones secretion. Intestinal microbiota includes trillions of microorganisms but its composition and function may be adversely affected in type 2 diabetes. The intestinal microbiota may be responsible of the secretion of molecules that may impair insulin secretion/action. At the same time, intestinal milieu regulates the secretion of hormones such as GLP-1, GIP, ghrelin, gastrin, somatostatin, CCK, serotonin, peptide YY, GLP-2, all of which importantly influence metabolism in general and in particular glucose metabolism. Thus, the aim of this paper is to review the current evidence on the role of the gut in the pathogenesis of type 2 diabetes, taking into account both hormonal and microbiological aspects

The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis

The widespread increase in life expectancy is accompanied by an increased prevalence of features of physical frailty. Signs and symptoms may include sarcopenia and osteopenia, reduced exercise capacity, and diminished sense of well-being. The pathogenesis of age-associated sarcopenia and osteopenia is multifactorial, and hormonal decline may be a contributing factor. Aging is associated with a progressive decrease in GH secretion, and more than 30% of elderly people have circulating IGF1 levels below the normal range found in the young. GH acts directly on target tissues, including skeletal muscle and bone among many others, but many effects are mediated indirectly by circulating (liver-derived) or locally produced IGF1. Aging is also associated with reduced insulin sensitivity which, in turn, may contribute to the impairment of IGF1 action. Recent experimental evidence suggests that besides the age-dependent decline in GH and IGF1 serum levels, the dysregulation of GH and IGF1 actions due to impairment of the post-receptor signaling machinery may contribute to the loss of muscle mass and osteopenia. This article will focus on the molecular mechanisms of impaired GH and IGF1 signaling and action in aging, and their role in the pathogenesis of sarcopenia and osteoporosis

Dehydroepiandrosterone Stimulates Glucose Uptake in Human and Murine Adipocytes by Inducing GLUT1 and GLUT4 Translocation to the Plasma Membrane

Dehydroepiandrosterone (DHEA) has been shown to modulate glucose utilization in humans and animals, but the mechanisms of DHEA action have not been clarified. We show that DHEA induces a dose- and time-dependent increase in glucose transport rates in both 3T3-L1 and human adipocytes with maximal effects at 2 h. Exposure of adipocytes to DHEA does not result in changes of total GLUT4 and GLUT1 protein levels. However, it does result in significant increases of these glucose transporters in the plasma membrane. In 3T3-L1 adipocytes, DHEA increases tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 and stimulates IRS-1- and IRS-2-associated phosphatidylinositol (PI) 3-kinase activity with no effects on either insulin receptor or Akt phosphorylation. In addition, DHEA causes significant increases of cytosolic Ca2+ concentrations and a parallel activation of protein kinase C (PKC)-β2. The effects of DHEA are abrogated by pretreatment of adipocytes with PI 3-kinase and phospholipase Cγ inhibitors, as well as by inhibitors of Ca2+-dependent PKC isoforms, including a specific PKC-β inhibitor. Thus, DHEA increases glucose uptake in both human and 3T3-L1 adipocytes by stimulating GLUT4 and GLUT1 translocation to the plasma membrane. PI 3-kinase, phospholipase Cγ, and the conventional PKC-β2 seem to be involved in DHEA effects

Long-term exposure of pancreatic β-cells to palmitate results in SREBP-1C-dependent decreases in GLP-1 receptor signaling via CREB and AKT and insulin secretory response

The effects of prolonged exposure of pancreatic β-cells to high saturated fatty acids on glucagonlike peptide-1 (GLP-1) action were investigated. Murine islets, human pancreatic 1.1B4 cells, and rat INS-1E cells were exposed to palmitate for 24 hours. mRNA and protein expression/phosphorylation were measured by real-time RT-PCR and immunoblotting, respectively. Specific short interfering RNAs were used to knockdown expression of the GLP-1 receptor (Glp1r) and Srebf1. Insulin release was assessed with a specific ELISA. Exposure of murine islets, as well as of human and INS-1E β-cells, to palmitate reduced the ability of exendin-4 to augment insulin mRNA levels, protein content, and release. In addition, palmitate blocked exendin-4-stimulated cAMP-response element-binding protein and v-akt murine thymoma viral oncogene homolog phosphorylation, whereas phosphorylation of MAPK-ERK kinase-1/2 and ERK-1/2 was not altered. Similarly, RNA interference-mediated suppression of Glp1r expression prevented exendin-4-induced cAMP-response element-binding protein and v-akt murine thymoma viral oncogene homolog phosphorylation, but did not impair exendin-4 stimulation of MAPK-ERK kinase-1/2 and ERK-1/2. Both islets from mice fed a high fat diet and human and INS-1E β-cells exposed to palmitate showed reduced GLP-1 receptor and pancreatic duodenal homeobox-1 (PDX-1) and increased sterol regulatory element-binding protein (SREBP-1C) mRNA and protein levels. Furthermore, suppression of SREBP-1C protein expression prevented the reduction of PDX-1 and GLP-1 receptor levels and restored exendin-4 signaling and action. Finally, treatment of INS-1E cells with metformin for 24 h resulted in inhibition of SREBP-1C expression, increased PDX-1 and GLP-1 receptor levels, consequently, enhancement of exendin-4-induced insulin release. Palmitate impairs exendin-4 effects on β-cells by reducing PDX-1 and GLP-1 receptor expression and signaling inaSREBP-1C-dependent manner. Metformin counteracts the impairment of GLP-1 receptor signaling induced by palmitate

TNFα signals via p66Shcto induce E-selectin, promote leukocyte transmigration and enhance permeability in human endothelial cells

Endothelial cells participate in inflammatory events leading to atherogenesis by regulating endothelial cell permeability via the expression of VE-Cadherin and β-catenin and leukocyte recruitment via the expression of E-Selectins and other adhesion molecules. The protein p66Shc acts as a sensor/inducer of oxidative stress and may promote vascular dysfunction. The objective of this study was to investigate the role of p66Shc in tumor necrosis factor TNFα-induced E-Selectin expression and function in human umbilical vein endothelial cells (HUVEC). Exposure of HUVEC to 50 ng/ml TNFα resulted in increased leukocyte transmigration through the endothelial monolayer and E-Selectin expression, in association with augmented phosphorylation of both p66Shc on Ser36 and the stress kinase c-Jun NH2-terminal protein kinase (JNK)-1/2, and higher intracellular reactive oxygen species (ROS) levels. Overexpression of p66 Shc in HUVEC resulted in enhanced p66Shc phosphorylation on Ser36, increased ROS and E-Selectin levels, and amplified endothelial cell permeability and leukocyte transmigration through the HUVEC monolayer. Conversely, overexpression of a phosphorylation-defective p66 Shc protein, in which Ser36 was replaced by Ala, did not augment ROS and E-Selectin levels, nor modify cell permeability or leukocyte transmigration beyond those found in wild-type cells. Moreover, siRNA-mediated silencing of p66Shc resulted in marked reduction of E-Selectin expression and leukocyte transmigration. In conclusion, p66Shc acts as a novel intermediate in the TNFα pathway mediating endothelial dysfunction, and its action requires JNK-dependent phosphorylation of p66 Shc on Ser36. © 2013 Laviola et al