Elena Silvestri

ORCID: 0000-0002-0592-9033
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Mitochondrial Function and Pathology
  • Thyroid Disorders and Treatments
  • Metabolism, Diabetes, and Cancer
  • Muscle metabolism and nutrition
  • Cancer, Hypoxia, and Metabolism
  • Biochemical effects in animals
  • Adipokines, Inflammation, and Metabolic Diseases
  • Growth Hormone and Insulin-like Growth Factors
  • Diet and metabolism studies
  • Metabolomics and Mass Spectrometry Studies
  • Fatty Acid Research and Health
  • Alzheimer's disease research and treatments
  • Metabolism and Genetic Disorders
  • ATP Synthase and ATPases Research
  • Peroxisome Proliferator-Activated Receptors
  • Sirtuins and Resveratrol in Medicine
  • Cardiovascular Disease and Adiposity
  • Pancreatic function and diabetes
  • Lipid metabolism and biosynthesis
  • Liver Disease Diagnosis and Treatment
  • Advanced Proteomics Techniques and Applications
  • Neuroscience and Neuropharmacology Research
  • Exercise and Physiological Responses
  • Dietary Effects on Health

University of Sannio
2014-2024

University of Florence
2020-2024

Hudson Institute
2017

University of Naples Federico II
2006-2008

Servei de Salut de les Illes Balears
2008

Research Institute of Health Sciences
2008

Universitat de les Illes Balears
2008

The overall effect of brain zinc (Zn2+) in the progression and development Alzheimer's disease (AD) is still not completely understood. Although an excess Zn2+ can exacerbate pathological features AD, a deficit intake has also been shown to increase volume amyloid plaques AD transgenic mice. In this study, we investigated dietary supplementation (30 p.p.m.) mouse model 3xTg-AD, that expresses both β (Aβ)- tau-dependent pathology. We found greatly delays hippocampal-dependent memory deficits...

10.1038/cddis.2010.73 article EN cc-by Cell Death and Disease 2010-10-28

Background The pathogenic road map leading to Alzheimer's disease (AD) is still not completely understood; however, a large body of studies in the last few years supports idea that beside classic hallmarks disease, namely accumulation amyloid-β (Aβ) and neurofibrillary tangles, other factors significantly contribute initiation progression disease. Among them, mitochondria failure, an unbalanced neuronal redox state, dyshomeostasis endogenous metals like copper, iron, zinc have all been...

10.1371/journal.pone.0017971 article EN cc-by PLoS ONE 2011-03-15

ABSTRACT The effect of thyroid hormones on metabolism has long supported their potential as drugs to stimulate fat reduction, but the concomitant induction a thyrotoxic state greatly limited use. Recent evidence suggests that 3,5‐diiodo‐ L ‐thyronine (T 2 ), naturally occurring iodothyronine, stimulates metabolic rate via mechanisms involving mitochondrial apparatus. We examined whether this would result in reduced energy storage. Here, we show T administration rats receiving high‐fat diet...

10.1096/fj.05-3977fje article EN The FASEB Journal 2005-07-12

OBJECTIVE High-fat diets (HFDs) are known to induce insulin resistance. Previously, we showed that 3,5-diiodothyronine (T2), concomitantly administered rats on a 4-week HFD, prevented gain in body weight and adipose mass. Here investigated whether how T2 HFD-induced RESEARCH DESIGN AND METHODS We the biochemical targets of related lipid glucose homeostasis over time using various techniques, including genomic proteomic profiling, immunoblotting, transient transfection, enzyme activity...

10.2337/db11-0207 article EN cc-by-nc-nd Diabetes 2011-09-17

Recent studies have shown that type 2 diabetes mellitus (T2DM) is a risk factor for cognitive dysfunction or dementia. Insulin resistance often associated with T2DM and can induce defective insulin signaling in the central nervous system as well increase of impairment elderly. Glucagone like peptide-1 (GLP-1) an incretin hormone and, GLP-1 analogs, stimulates secretion has been employed treatment T2DM. analogs also enhance synaptic plasticity counteract deficits mouse models neuronal and/or...

10.1038/cddis.2013.139 article EN cc-by Cell Death and Disease 2013-05-02

Metabolic dysfunction-associated fatty liver disease (MAFLD) is defined as the presence of hepatic steatosis in addition to one three metabolic conditions: overweight/obesity, type 2 diabetes mellitus, or dysregulation. Chronic exposure excess dietary acids may cause and disturbances. The alteration quality mitochondria factors that could contribute dysregulation MAFDL. This study was designed determine, a rodent model MAFLD, effects long-term high-fat diet (HFD) on some processes...

10.3390/genes13020315 article EN Genes 2022-02-08

Thyroid hormones increase energy expenditure, partly by reducing metabolic efficiency. The control of specific genes at the transcriptional level is thought to be major molecular mechanism. However, both number and identity thyroid hormone-controlled remain unknown, as do their relative contributions. Uncoupling protein-3, a recently identified member mitochondrial transporter superfamily one that predominantly expressed in skeletal muscle, has potential determinant for thermogenesis....

10.1210/endo.142.8.8303 article EN Endocrinology 2001-08-01

Triiodothyronine regulates energy metabolism and thermogenesis. Among triiodothyronine derivatives, 3,5-diiodo-l-thyronine (T 2 ) has been shown to exert marked effects on by acting mainly at the mitochondrial level. Here we investigated capacity of T affect both skeletal muscle substrate oxidation thermogenesis within 1 h after its injection into hypothyroid rats. Administration induced an increase in when palmitoyl-CoA (+104%), palmitoylcarnitine (+80%), or succinate (+30%) was used as...

10.1152/ajpendo.90642.2008 article EN AJP Endocrinology and Metabolism 2008-12-31

The worldwide prevalence of obesity-associated pathologies, including type 2 diabetes, requires thorough investigation mechanisms and interventions. Recent studies have highlighted thyroid hormone analogs derivatives as potential agents able to counteract such pathologies. In this study, in rats receiving a high-fat diet (HFD), we analyzed the effects 4-wk daily administration naturally occurring iodothyronine, 3,5-diiodo-L-thyronine (T2), on gastrocnemius muscle metabolic/structural...

10.1096/fj.11-181982 article EN The FASEB Journal 2011-06-13

In this study, we investigated the effects of long-term (9-month) treatment with pioglitazone (PIO; 20 mg/kg/d) in two animal models Alzheimer's disease (AD)-related neural dysfunction and pathology: PS1-KIM146V (human presenilin-1 M146V knock-in mouse) 3xTg-AD (triple transgenic mouse carrying AD-linked mutations) mice. We also on wild-type (WT) Mice were monitored for body mass changes, fasting glycemia, glucose tolerance, studied changes brain mitochondrial enzyme activity (complexes I...

10.1038/cddis.2012.189 article EN cc-by Cell Death and Disease 2012-12-20

Because we previously reported that T3 and 3,5-diiodo-L-thyronine (3,5-T2) both increase resting metabolic rate (RMR), 3,5-T2 could be another thyroidal regulator of energy metabolism. This effect is evident in rats made hypothyroid by propylthiouracil iopanoic acid, not normal euthyroid (N) rats. Possibly, under conditions, active may need to formed intracellularly from a precursor such as T3. We tested this hypothesis giving single injection N comparing the time course variations RMR with...

10.1210/endo.143.2.8613 article EN Endocrinology 2002-02-01

Coping with reduced energy sources entails drastic morphological and functional changes in skeletal muscle, but the sequence of events required classification. We found that gastrocnemius muscle from food-deprived rats shows acute rises peroxisome proliferator activated receptor (PPAR) gamma coactivator (PGC) -1alpha/PPAR delta nuclear protein myosin heavy chain (MHC) Ib protein, while type I fibers accumulate tissue appears redder. AMP levels, phosphorylation both AMP-activated kinase...

10.1096/fj.06-6025fje article EN The FASEB Journal 2006-10-25

Peroxisome proliferator-activated receptors (PPARs), which are known to regulate lipid homeostasis, tightly controlled by nutrient availability, and they control handling. In this paper, we focus on how nutrients the expression action of PPARs cellular signaling events in metabolically active tissues (e.g., liver, skeletal muscle, heart, white adipose tissue). We address structure function PPARs, their interaction with other nuclear receptors, including PPAR cross-talk. further discuss roles...

10.1155/2010/435689 article EN cc-by PPAR Research 2010-01-01

The triple-transgenic Alzheimer (3 × Tg-AD) mouse expresses mutant PS1M146V, APPswe, and tauP301L transgenes progressively develops plaques neurofibrillary tangles with a temporal- region-specific profile that resembles the neuropathological progression of Alzheimer's disease (AD). In this study, we used proteomic approaches such as two-dimensional gel electrophoresis mass spectrometry to investigate alterations in protein expression occurring brain cerebellum 3 Tg-AD presenilin-1 (PS1)...

10.1038/cddis.2010.68 article EN cc-by Cell Death and Disease 2010-10-28

We evaluated the effects of fasting on gene expression profile in rat gastrocnemius muscle using a combined cDNA array and RT-PCR approach. Of 1176 distinct genes analyzed array, 114 were up-regulated more than twofold response to fasting, including all 17 related lipid metabolism present membranes 10 components proteasome machinery. Only 7 down-regulated twofold. On basis our analysis plus data from assays, metabolic adaptations shown by during are reflected i) increased transcription both...

10.1096/fj.03-0342fje article EN The FASEB Journal 2003-12-04
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