Neuregulin 4 (Nrg4) is an adipokine that belongs to the epidermal growth factor family and binds to ErbB4 tyrosine kinase receptors. In 3T3-L1 adipocytes, the downregulation of expression enhances inflammation and autophagy, resulting in insulin resistance. Here, we searched for the causes of this phenotype.
View Article and Find Full Text PDFBrown adipose tissue (BAT) thermogenesis affects energy balance, and thereby it has the potential to induce weight loss and to prevent obesity. Here, we document a macroautophagic/autophagic-dependent mechanism of peroxisome proliferator-activated receptor gamma (PPARG) activity regulation that induces brown adipose differentiation and thermogenesis and that is mediated by TP53INP2. Disruption of TP53INP2-dependent autophagy reduced brown adipogenesis in cultured cells.
View Article and Find Full Text PDFExtracellular vesicles (EVs) are membrane enclosures released by eukaryotic cells that carry bioactive molecules and serve to modulate biological responses in recipient cells. Both increased EV release and altered EV composition are associated with the development and progression of many pathologies including cancer. Hypoxia, a feature of rapidly growing solid tumours, increases the release of EVs.
View Article and Find Full Text PDFAims: To test the hypothesis that adipose tissue gene expression patterns would be affected by metabolic surgery and we aimed to identify genes and metabolic pathways as well as metabolites correlating with metabolic changes following metabolic surgery.
Materials And Methods: This observational study was conducted at the Obesity Unit at the Catholic University Hospital of the Sacred Heart in Rome, Italy. Fifteen patients, of which six patients underwent Roux-en-Y gastric bypass and nine patients underwent biliopancreatic diversion, were included.
The adipokine Neuregulin 4 (Nrg4) protects against obesity-induced insulin resistance. Here, we analyze how the downregulation of Nrg4 influences insulin action and the underlying mechanisms in adipocytes. Validated shRNA lentiviral vectors were used to generate scramble (Scr) and Nrg4 knockdown (KD) 3T3-L1 adipocytes.
View Article and Find Full Text PDFIntroduction: CoV-2 infection generates a pro-inflammatory state, which conditions the formation of thrombi that can affect any system. Multi-organ dysfunction is a cause of death, mesenteric ischemia in COVID 2019 patients reported is 1.9-4%.
View Article and Find Full Text PDFIntroduction: Inflammatory myofibroblastic tumors are neoplasms that occur infrequently, mainly affects children and young adults. It is an intermediate grade fibrotic multinodular neoplasm.
Description Of The Case: We present the case of a 47-year-old female patient, who underwent emergency umbilical hernioplasty, later developed intestinal obstruction secondary to an inflammatory myofibroblastic tumor.
Autophagy plays a key role in cellular homeostasis since it allows optimal cellular functioning and provides energy under conditions of stress. Initial is revealed that alterations of macroautophagy disturb adipogenic differentiation in cultured cells, and in mice, leading to a drastic reduction of adipose tissue depots. Nevertheless, more recent studies indicate that autophagy participates in the control of adipose tissue biology in a more complex manner.
View Article and Find Full Text PDFOpa1 participates in inner mitochondrial membrane fusion and cristae morphogenesis. Here, we show that muscle-specific Opa1 ablation causes reduced muscle fiber size, dysfunctional mitochondria, enhanced Fgf21, and muscle inflammation characterized by NF-κB activation, and enhanced expression of pro-inflammatory genes. Chronic sodium salicylate treatment ameliorated muscle alterations and reduced the muscle expression of Fgf21.
View Article and Find Full Text PDFExcessive fat accumulation is a major risk factor for the development of type 2 diabetes mellitus and other common conditions, including cardiovascular disease and certain types of cancer. Here, we identify a mechanism that regulates adiposity based on the activator of autophagy TP53INP2. We report that TP53INP2 is a negative regulator of adipogenesis in human and mouse preadipocytes.
View Article and Find Full Text PDFStudy Objectives: To develop the Barcelona Sleepiness Index (BSI), an interviewer-administered instrument for assessing excessive daytime sleepiness (EDS) in sleep-disordered breathing (SDB) that correlates well with objective measures of EDS and which is sensitive to change with treatment.
Methods: (1) Generation of a preliminary item list: Fifty-three consecutive SDB patients complaining of EDS and their bed partners were interviewed using a focus group methodology to generate a list of situations prone to cause sleepiness. Sixty different consecutive SDB patients were then evaluated using cognitive interviews to refine this list.
Parathyroid hormone-related protein (PTHrP) and its receptor type 1 (PTH1R) are extensively expressed in the kidney, where they are able to modulate renal function. Renal PTHrP is known to be overexpressed in acute renal injury. Recently, we hypothesized that PTHrP involvement in the mechanisms of renal injury might not be limited to conditions with predominant damage of the renal tubulointerstitium and might be extended to glomerular diseases, such as diabetic nephropathy (DN).
View Article and Find Full Text PDFHypertrophy of human mesangial cells (HMC) is among the earliest characteristics in patients with diabetic nephropathy (DN). Recently, we observed the upregulation of parathyroid hormone (PTH)-related protein (PTHrP) in experimental DN, associated with renal hypertrophy. Herein, we first examined whether PTHrP was overexpressed in human DN, and next assessed the putative role of this protein on high glucose (HG)-induced HMC hypertrophy.
View Article and Find Full Text PDFBackground: Hypertrophy of podocytes is characteristic in diabetic nephropathy (DN). Previously, we observed the upregulation of parathyroid hormone-related protein (PTHrP) and its receptor PTH1R, in experimental DN, associated with renal hypertrophy. Herein, we test the hypothesis that PTHrP participates in the mechanism of high glucose (HG)-induced podocyte hypertrophy.
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