Fernando Goglia

ORCID: 0000-0003-0468-9645
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About
Contact & Profiles
Research Areas
  • Adipose Tissue and Metabolism
  • Mitochondrial Function and Pathology
  • Thyroid Disorders and Treatments
  • Biochemical effects in animals
  • Muscle metabolism and nutrition
  • Growth Hormone and Insulin-like Growth Factors
  • Cancer, Hypoxia, and Metabolism
  • Metabolism, Diabetes, and Cancer
  • Adipokines, Inflammation, and Metabolic Diseases
  • Metabolism and Genetic Disorders
  • Liver Disease Diagnosis and Treatment
  • Diet and metabolism studies
  • Nitric Oxide and Endothelin Effects
  • Peroxisome Proliferator-Activated Receptors
  • Metabolomics and Mass Spectrometry Studies
  • Diet, Metabolism, and Disease
  • Fatty Acid Research and Health
  • ATP Synthase and ATPases Research
  • Exercise and Physiological Responses
  • Regulation of Appetite and Obesity
  • Sirtuins and Resveratrol in Medicine
  • High Altitude and Hypoxia
  • Cardiovascular Disease and Adiposity
  • Lipid metabolism and biosynthesis
  • Neuroscience and Neuropharmacology Research

University of Sannio
2016-2025

Istituti Clinici Scientifici Maugeri
2020

University of Naples Federico II
1997-2012

Istituto Nazionale Biostrutture e Biosistemi
2011

Research Institute of Health Sciences
2008

Universitat de les Illes Balears
2008

Servei de Salut de les Illes Balears
2008

University of Genoa
2001

Istituto Nazionale di Fisica Nucleare, Sezione di Napoli
1980

It is hypothesized that mitochondrial uncoupling proteins operate as carriers of fatty acid peroxide anions. This assumed to result in electrophoretic extrusion such anions from the inner outer leaflet membrane, being driven by membrane potential (mitochondrial interior negative). In this way, ridded peroxides otherwise can form very aggressive oxidants damaging DNA, aconitase, and other matrix-localized components vital importance. The steady-state concentration known be low. explains why...

10.1096/fj.03-0159hyp article EN The FASEB Journal 2003-09-01

The short‐term effects of thyroid hormones, which do not occur via gene expression, were postulated to be based on interaction diiodothyronines with mitochondria. We demonstrate specific binding labelled 3,5‐diiodothyronine subunit Va cytochrome‐ c oxidase from bovine heart. 3,5‐Diiodothyronine, and a small extent triiodothyronine, but thyroxine thyronine, abolish the allosteric inhibition ascorbate respiration reconstituted cytochrome by ATP [Arnold, S. & Kadenbach, B. (1997) Eur. J....

10.1046/j.1432-1327.1998.2520325.x article EN European Journal of Biochemistry 1998-03-01

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

Distinct brain peptidergic circuits govern peripheral energy homeostasis and related behavior. Here we report that mitochondrial uncoupling protein 2 (UCP2) is expressed discretely in neurons involved homeostatic regulation. UCP2 was associated with the mitochondria of neurons, predominantly axons axon terminals. UCP2-producing were found to be targets hormones, including leptin gonadal steroids, presence axonal processes predicted increased local activity heat production. In hypothalamus,...

10.1523/jneurosci.19-23-10417.1999 article EN cc-by-nc-sa Journal of Neuroscience 1999-12-01

The importance of local formation T3 in the feedback effect thyroid gland on hypothalamic TRH-producing cells has been established. Primary failure results a fall circulating T4 and levels, leading to an elevation production release TRH paraventricular nucleus. In contrast, during short term fasting, declining plasma levels hormones coincide with suppressed release. brain, prevalent enzyme that converts is type II iodothyronine deiodinase (DII). present study was undertaken determine whether...

10.1210/endo.139.6.6062 article EN Endocrinology 1998-06-01

Fibrates are hypolipidemic drugs that activate the peroxisome proliferator‐activated receptors. Since fibrates may also increase energy expenditure, we investigated whether fenofibrate (FF) had this effect in diet‐induced obese rats. A 2‐month administration of a high‐fat palatable diet to adult rats increased body weight by 25% and white adipose mass 163% compared with standard diet. These effects were prevented FF, both when administered for 2 months feeding given only second month....

10.1016/s0014-5793(01)02146-9 article EN FEBS Letters 2001-02-20

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

Although the first evidence of a relationship between thyroid and metabolism was reported in 1895, mechanism by which hormones influence resting metabolic rate whole animals is still poorly understood. This paper reports an attempt to test whether diiodothyronines (T 2 s) triiodothyronine 3 ) have different roles control (RM). Changes were measured hypothyroid rats treated acutely (25μg (100 g body weight) −1 either with one T s or . Injection induced increase about 35% RM that started 25–30...

10.1111/j.1469-7793.1997.529bb.x article EN The Journal of Physiology 1997-12-01

An increased prevalence of type 2 diabetes and impaired glucose tolerance has been consistently found in liver cirrhosis from any cause (1–3). Less clear is whether hepatitis C virus (HCV) infection associated with the absence cirrhosis. Several reports have claimed a specific association between HCV diabetes, but most instances, patients were mixture cases (4–6). Two clinic-based studies an excess noncirrhotic HCV+ (NC-HCV+) compared chronic other origin (7–9), another large study could not...

10.2337/diacare.28.10.2548 article EN Diabetes Care 2005-10-01

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

Evidence indicates that many forms of fructose-induced metabolic disturbance are associated with oxidative stress and mitochondrial dysfunction. Mitochondria prominent targets damage; however, it is not clear whether DNA (mtDNA) damage and/or its lack repair events involved in disease resulting from a fructose-rich diet. In the present study, we evaluated degree to liver mtDNA repair, addition state antioxidant defense rats fed high-fructose We used male feeding on or control diet for eight...

10.3390/nu9040323 article EN Nutrients 2017-03-24

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

We sought a correlation between rat skeletal muscle triiodothyronine (T3)‐mediated regulation of uncoupling protein‐3 (UCP3) expression and mitochondrial activity. UCP3 mRNA increased strongly during the hypothyroid‐hyperthyroid transition. The rank order State 3 4 respiration rates was hypothyroid<euthyroid<hyperthyroid. increase may have been due to expression, as proton leak kinetic stimulated in transition good exists level. As significant proportion an organism's resting oxygen...

10.1016/s0014-5793(99)00061-7 article EN FEBS Letters 1999-02-12

The possible regulation of the expression uncoupling protein-2 (UCP2) mRNA by thyroid hormones in different tissues was examined rats. Triiodothyronine (T3) found to produce an organ-specific enhancement UCP2 rat tissues. effect T3 markedly observed heart, whereas a moderate seen skeletal muscle and no kidney or liver. These results suggest that is protein may be involved nuclear-mediated on resting metabolic rate rat.

10.1016/s0014-5793(97)01375-6 article EN FEBS Letters 1997-11-24
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