Perceived health status: is obesity perceived as a risk factor and disease?

One might expect that a perception of obesity being a risk factor and disease, contributes to effective obesity prevention and management strategies. However, obesity rates continue to increase worldwide. The question arises whether obesity is truly perceived as a risk factor and a disease. This paper aims at describing perception of obesity as risk factor and disease among individuals seeking care, individuals not seeking care, the society, and different professionals having a role in the field of obesity. The paper is a reflection of the lecture on the topic that was given at the EASO's New Investigators United's Summer School 2016 in Portugal and the discussion with the new investigators and other senior speakers. Individual obese patients seeking help are very much aware of obesity being a risk factor and disease, but perceptions regarding obesity seem to be flawed among those who do not seek help for obesity. Also, misperceptions regarding obesity play a role at different levels, including society, different political levels, the fields of health care and social work, prevention organizations, and the food and marketing industry. The food and marketing industry has an enormous role in changing perceptions by the society and policy makers. Obesity rates will continue to increase as long as individuals, the society, and professionals at different levels have false interpretations of the severity of obesity. Severe action is needed against those who are playing a role in maintaining false perceptions of obesity as a risk factor and disease.- (undefined

Hemivulvectomía radical por gangrena de fournier en mujer con antecedente de radioterapia pélvica

The Fournier’s Gangrene is a necrotizing infection which is located in the perineal area. It ́s a severe infection, which involves a quick evolution to advanced stages where a high morbimortality rate is associated. However, it often tends to be underdiagnosed in early stages. The most important in the diagnosis is a high clinical suspicion and subsequent surgical treatment which is base on a desbridalment and exeresis of the affected tissues. In addition, the association of broad-spectrum antibiotic therapy and nutritional support are crucial. This report reviews a clinical case of Fournier's Gangrene, in a patient with a history of radiation induced cystitis and pubic osteitis after pelvic radiotherapy, diagnosed and treated with a radical hemivulvectomy, antibiotic therapy and lavages in our Hospital

Implication of ghrelin isoforms in the improvement of nonalcoholic fatty liver disease after bariatric surgery

Bariatric surgery improves NAFLD and NASH, but the underlying mechanisms remain unknown. The present thesis shows the potential role of acylated and desacyl ghrelin in the progression of NAFLD to NASH through the amelioration of hepatic steatosis and inflammation after bariatric surgery in an experimental model of obesity as well as in patients with morbid obesity. Diet-induced obese rats developed hepatosteatosis and showed decreased circulating desacyl ghrelin without changes in acylated ghrelin concentrations. Sleeve gastrectomy and RYGB induced a dramatic reduction in desacyl ghrelin levels, whereas the acylated/desacyl ghrelin ratio was augmented in obese rats. In patients with morbid obesity and NAFLD, desacyl ghrelin levels were diminished, while circulating TNF-α and the acylated/desacyl ghrelin ratio were increased. Interestingly, six months after bariatric surgery, decreased acylated/desacyl ghrelin levels were found in morbidly obese patients. We demonstrated that bariatric surgery improved hepatic steatosis by reducing hepatic TG content and the lipogenic enzymes Mogat2 and Dgat1, and triggering AMPK-activated mitochondrial FFA β-oxidation and autophagy to a higher extent than caloric restriction in diet-induced obese rats. In addition, both sleeve gastrectomy and RYGB ameliorated hepatic inflammation, as evidenced by a decrease in portal and lobulillar CD68+ and apoptotic cells, proinflammatory JNK activation and a downregulation in the expression of inflammation-related genes (Crp, Tnf and Il6). In parallel, mitochondrial dysfunction was significantly attenuated after sleeve gastrectomy and RYGB via an increase in mitochondrial DNA amount as well as OXPHOS complexes I and II together with an amelioration of ER stress. Specifically, GRP78, spliced XBP-1, ATF4 and CHOP levels were reduced, as was phosphorylated eIF2α, following both bariatric surgical procedures. Our results show that the stimulation of primary rat hepatocytes with acylated and desacyl ghrelin significantly increased TG content, but also prompted AMPK-activated mitochondrial FFA β-oxidation and autophagy. Furthermore, acylated and desacyl ghrelin also inhibited palmitate-triggered inflammation and UPR induction through the downregulation of IRE1α, PERK and ATF6 expression as well as their downstream effectors, ATF4 and CHOP, and chaperone GRP78. In human HepG2 hepatocytes, acylated and desacyl ghrelin treatment reduced TNF-α-induced apoptosis, evidenced by lower caspase-8 and caspase-3 cleavage, as well as TUNEL-positive cells and pyroptosis, revealed by decreased caspase-1 activation and lower HMGB1 expression. Moreover, acylated ghelin suppressed TNF-α-activated hepatocyte autophagy, supported by decreased LC3B-II/I ratio and increased p62 accumulation via AMPK/mTOR, with acylated ghrelin being a protective factor against hepatocyte cell death. Thus, the decrease in the most abundant isoform, desacyl ghrelin, after bariatric surgery contributes to the reduction of lipogenesis, whereas the increased relative acylated ghrelin levels activate factors involved in mitochondrial FFA β-oxidation and autophagy as well as contribute to mitigate obesity-associated hepatic inflammation, mitochondrial dysfunction, ER stress and cell death, thereby ameliorating NAFL

Implication of ghrelin isoforms in the improvement of nonalcoholic fatty liver disease after bariatric surgery

Bariatric surgery improves NAFLD and NASH, but the underlying mechanisms remain unknown. The present thesis shows the potential role of acylated and desacyl ghrelin in the progression of NAFLD to NASH through the amelioration of hepatic steatosis and inflammation after bariatric surgery in an experimental model of obesity as well as in patients with morbid obesity. Diet-induced obese rats developed hepatosteatosis and showed decreased circulating desacyl ghrelin without changes in acylated ghrelin concentrations. Sleeve gastrectomy and RYGB induced a dramatic reduction in desacyl ghrelin levels, whereas the acylated/desacyl ghrelin ratio was augmented in obese rats. In patients with morbid obesity and NAFLD, desacyl ghrelin levels were diminished, while circulating TNF-α and the acylated/desacyl ghrelin ratio were increased. Interestingly, six months after bariatric surgery, decreased acylated/desacyl ghrelin levels were found in morbidly obese patients. We demonstrated that bariatric surgery improved hepatic steatosis by reducing hepatic TG content and the lipogenic enzymes Mogat2 and Dgat1, and triggering AMPK-activated mitochondrial FFA β-oxidation and autophagy to a higher extent than caloric restriction in diet-induced obese rats. In addition, both sleeve gastrectomy and RYGB ameliorated hepatic inflammation, as evidenced by a decrease in portal and lobulillar CD68+ and apoptotic cells, proinflammatory JNK activation and a downregulation in the expression of inflammation-related genes (Crp, Tnf and Il6). In parallel, mitochondrial dysfunction was significantly attenuated after sleeve gastrectomy and RYGB via an increase in mitochondrial DNA amount as well as OXPHOS complexes I and II together with an amelioration of ER stress. Specifically, GRP78, spliced XBP-1, ATF4 and CHOP levels were reduced, as was phosphorylated eIF2α, following both bariatric surgical procedures. Our results show that the stimulation of primary rat hepatocytes with acylated and desacyl ghrelin significantly increased TG content, but also prompted AMPK-activated mitochondrial FFA β-oxidation and autophagy. Furthermore, acylated and desacyl ghrelin also inhibited palmitate-triggered inflammation and UPR induction through the downregulation of IRE1α, PERK and ATF6 expression as well as their downstream effectors, ATF4 and CHOP, and chaperone GRP78. In human HepG2 hepatocytes, acylated and desacyl ghrelin treatment reduced TNF-α-induced apoptosis, evidenced by lower caspase-8 and caspase-3 cleavage, as well as TUNEL-positive cells and pyroptosis, revealed by decreased caspase-1 activation and lower HMGB1 expression. Moreover, acylated ghelin suppressed TNF-α-activated hepatocyte autophagy, supported by decreased LC3B-II/I ratio and increased p62 accumulation via AMPK/mTOR, with acylated ghrelin being a protective factor against hepatocyte cell death. Thus, the decrease in the most abundant isoform, desacyl ghrelin, after bariatric surgery contributes to the reduction of lipogenesis, whereas the increased relative acylated ghrelin levels activate factors involved in mitochondrial FFA β-oxidation and autophagy as well as contribute to mitigate obesity-associated hepatic inflammation, mitochondrial dysfunction, ER stress and cell death, thereby ameliorating NAFL

Effects of diets on adipose tissue

Obesity is a major health problem that has become a global epidemic. Overweight and obesity are commonly associated with the development of several pathologies, such as insulin resistance, cardiovascular diseases, sleep apnea and several types of cancer, which can lead to further morbidity and mortality. An increased abdominal adiposity renders overweight and obese individuals more prone to metabolic and cardiovascular problems. In this sense, excess adiposity leads to several changes in the biology, morphology and function of the adipose tissue, such as adipocyte hypertrophy and hyperplasia, adipose tissue inflammation and fibrosis and an impaired secretion of adipokines, contributing to the onset of obesity-related co-morbidities. Given the medical, social and economic consequences of obesity, there is an urgent need to develop strategies to deal with this epidemic. The first approach for obesity management and prevention is the implementation of a diet combined with physical activity. Dietary changes should be individualised, tailored to food preferences and allow for flexible approaches to reducing calorie intake in order to increase the motivation and compliance of overweight and obese patients. The present review summarizes the compelling evidence showing body composition changes, impact on cardiometabolism and potential adverse effects of very-low calorie, low- and high-carbohydrate, high-protein or low-fat diets. The use of macronutrients during the preprandial and postprandial state has been also reviewed to better understand the metabolic changes induced by different dietary interventions

Pancreatic Aquaporin-7: A Novel Target for Anti-diabetic Drugs?

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role of aquaporins in the physiology and pathophysiology of the pancreas, highlighting the role of pancreatic AQP7 as a novel player in the control of β-cell function and a potential anti-diabetic-drug

Pancreatic aquaporin-7: a novel target for anti-diabetic drugs?

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role of aquaporins in the physiology and pathophysiology of the pancreas, highlighting the role of pancreatic AQP7 as a novel player in the control of β-cell function and a potential anti-diabetic-drug

Pancreatic aquaporin-7: a novel target for anti-diabetic drugs?

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role of aquaporins in the physiology and pathophysiology of the pancreas, highlighting the role of pancreatic AQP7 as a novel player in the control of β-cell function and a potential anti-diabetic-drug

Pancreatic Aquaporin-7: A Novel Target for Anti-diabetic Drugs?

Aquaporins comprise a family of 13 members of water channels (AQP0-12) that facilitate a rapid transport of water across cell membranes. In some cases, these pores are also permeated by small solutes, particularly glycerol, urea or nitric oxide, among other solutes. Several aquaporins have been identified in the pancreas, an exocrine and endocrine organ that plays an essential role in the onset of insulin resistance and type 2 diabetes. The exocrine pancreas, which accounts for 90% of the total pancreas, secretes daily large volumes of a near-isotonic fluid containing digestive enzymes into the duodenum. AQP1, AQP5, and AQP8 contribute to fluid secretion especially from ductal cells, whereas AQP12 allows the proper maturation and exocytosis of secretory granules in acinar cells of the exocrine pancreas. The endocrine pancreas (10% of the total pancreatic cells) is composed by the islets of Langerhans, which are distributed in α, β, δ, ε, and pancreatic polypeptide (PP) cells that secrete glucagon, insulin, somatostatin, ghrelin and PP, respectively. AQP7, an aquaglyceroporin permeated by water and glycerol, is expressed in pancreatic β-cells and murine studies have confirmed its participation in insulin secretion, triacylglycerol synthesis and proliferation of these endocrine cells. In this regard, transgenic AQP7-knockout mice develop adult-onset obesity, hyperinsulinemia, increased intracellular triacylglycerol content and reduced β-cell mass in Langerhans islets. Moreover, we have recently reported that AQP7 upregulation in β-cells after bariatric surgery, an effective weight loss surgical procedure, contributes, in part, to the improvement of pancreatic steatosis and insulin secretion through the increase of intracytoplasmic glycerol in obese rats. Human studies remain scarce and controversial, with some rare cases of loss-of function mutations of the AQP7 gene being associated with the onset of type 2 diabetes. The present Review is focused on the role of aquaporins in the physiology and pathophysiology of the pancreas, highlighting the role of pancreatic AQP7 as a novel player in the control of β-cell function and a potential anti-diabetic-drug

The Potential of Satellite Interferometry for Geohazard Assessment in Cultural Heritage Sites

[EN] A continuous monitoring system of ground deformation, based on radar images acquired by ESA (European Space Agency) Sentinel-1 constellation, is active over the Tuscany Region (Central Italy). The potential of repeat-pass satellite SAR (Synthetic Aperture Radar) interferometry has been exploited to investigate spatial patterns and temporal evolution of regional and local ground deformation that affect cultural heritage sites. With millions of measurement points, ground deformation maps for Tuscany Region provide information that can be exploited to scan wide areas and to flag ground instabilities. These areas become targets for detailed analysis with high resolution sensors (e.g., COSMO-SkyMed satellites of the Italian Space Agency) to create a virtual constellation, in which different satellite data sources are synergically used to create a more effective and robust Earth Observation system. The potential of a virtual constellation is presented and discussed through the case study of Pistoia, a city whose origins date back to the Etruscan civilization.The ground deformation monitoring system presented in this paper has been requested, founded and supported by the Regional government of Tuscany, under the agreement “Monitoring ground deformation in the Tuscany Region with satellite radar data”.Peer reviewe