Francesco Fantin

Prof. Francesco Fantin

Department of Medicine, Section of Geriatric Medicine, Piazzale Stefani 1, University of Verona, 37126 Verona, Italy
orcid

Research Focus & Metrics

Academic Career Length

23Years (2004-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2008 in Nutrition, Metabolism and Cardiovascular Diseases
Verified
Journal Article
Closed access
MZMauro Zamboni
Mauro Zamboni
GMGloria Mazzali
Gloria Mazzali
FFFrancesco Fantin
Francesco Fantin
ARAndrea Rossi
Andrea Rossi
VFVincenzo Di Francesco
Vincenzo Di Francesco

31 May 2005 in International Journal of Obesity
Verified
Journal Article
Closed access
MZMauro Zamboni
Mauro Zamboni
GMG Mazzali
G Mazzali
EZElena Zoico
Elena Zoico
THT B Harris
T B Harris
JMJ B Meigs
J B Meigs
OBO Bosello
O Bosello

20 June 2019 in Frontiers in Endocrinology
Verified
Journal Article
Open access
PDF file
EZElena Zoico
Elena Zoico
SRSofia Rubele
Sofia Rubele
ACAnnamaria De Caro
Annamaria De Caro
NNNicole Nori
Nicole Nori
GMGloria Mazzali
Gloria Mazzali
MZMauro Zamboni
Mauro Zamboni
Across aging, adipose tissue (AT) changes its quantity and distribution: AT becomes dysfunctional with an increase in production of inflammatory peptides, a decline of those with anti-inflammatory activity and infiltration of macrophages. Adipose organ dysfunction may lead to age-related metabolic alterations. Aging is characterized by an increase in adiposity and a decline in brown adipose tissue (BAT) depots and activity, and UCP1 expression. There are many possible links to age-associated involution of BAT, including the loss of mitochondrial function, impairment of the sympathetic nervous system, age-induced alteration of brown adipogenic stem/progenitor cell function and changes in endocrine signals. Aging is also associated with a reduction in beige adipocyte formation. Beige adipocytes are known to differentiate from a sub-population of progenitors resident in white adipose tissue (WAT); a defective ability of progenitor cells to proliferate and differentiate has been hypothesized with aging. The loss of beige adipocytes with age may be caused by changes in trophic factors in the adipose tissue microenvironment, which regulate progenitor cell proliferation and differentiation. This review focuses on possible mechanisms involved in the reduction of BAT and beige activity with aging, along with possible targets for age-related metabolic disease therapy.

28 October 2009 in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences
Verified
Journal Article
Open access
PDF file
EZElena Zoico
Elena Zoico
ARAndrea Rossi
Andrea Rossi
VFVincenzo Di Francesco
Vincenzo Di Francesco
ASAnna Sepe
Anna Sepe
DODebora Olioso
Debora Olioso
MZMauro Zamboni
Mauro Zamboni
Association between inflammatory markers and intermuscular adipose tissue (IMAT) has been reported. We hypothesized that subclinical inflammation of adipose tissue surrounding and infiltrating muscle could be related to the metabolic and functional abnormalities of the “aging muscle.” In 20 healthy elderly men undergoing elective vertebral surgery, IMAT within erector spinae was evaluated by magnetic resonance imaging and body composition by dual-energy x-ray absorptiometry. Fasting glucose, insulin, high-sensitive C-reactive protein (hs-CRP), leptin, adiponectin, and interleukin 6 (IL-6) were measured, and insulin resistance was estimated by homeostasis model assessment (HOMA) index. In subcutaneous adipose tissue (SAT) biopsies near the erector spinae, quantification of gene expression was performed. IMAT showed a significant association with body mass index and total and regional body fat, even after adjustment for age. Insulin, HOMA, and leptin were significantly correlated with IMAT, whereas hs-CRP presented an association of borderline significance. IL-6 expression in SAT was significantly associated with IMAT; IL-6 messenger RNA (mRNA) was negatively associated with adiponectin and peroxisome proliferator–activated receptor gamma expression. In multivariate regression analysis, 68% of IMAT variance was explained by fat mass and age, independent of waist circumference, leptin, HOMA, and IL-6 mRNA. IMAT was primarily related to age and total body adiposity; subclinical inflammation in fat significantly contributes to IMAT.

17 November 2006 in Age and Ageing
Verified
Journal Article
Open access
PDF file
FFFrancesco Fantin
Francesco Fantin
AMAdriana Mattocks
Adriana Mattocks
CBChristopher J. Bulpitt
Christopher J. Bulpitt
WBWinston Banya
Winston Banya
CRChakravarthi Rajkumar
Chakravarthi Rajkumar
Objectives we investigated the exact relationship between age and gender on augmentation pressure (AG) and augmentation index (AI) measured over the radial (muscular) and carotid (elastic) arteries. Design and Methods AG is the contribution that wave reflection makes to systolic arterial pressure. AI is an indirect measure of arterial stiffness and is calculated as AG divided by pulse pressure (PP) ×100. AG and AI both increase with age. AG and AI were measured in 458 subjects using SphygmoCor. A total of 755 readings were obtained (302 carotid, 453 radial). The mean age was 57.5 ± 13.7 years. Diabetic subjects were excluded. Among the subjects, 13.5% were hypertensive. Results statistically, women had mean values of AI significantly higher than men in both radial and carotid arteries. These differences were less marked with AG. Quadratic equations better described the relationship between AI and age but not AG and age. Thus, AI increased with age up to our median age of 55 years but plateaued thereafter, whereas the AG continued to increase steadily with age. A multiple regression analysis demonstrated that both AI and AG were negatively related to height and positively related to diastolic blood pressure (DBP). Conclusions AG continues to increase in the elderly over the age of 55, but not AI. AI is higher in women and higher when measured over the carotid than the radial. AI is positively related to DBP and negatively to height. AG is proposed as a more suitable measure of arterial stiffness than AI.

1 December 2007 in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences
Verified
Journal Article
Open access
PDF file
FFFrancesco Fantin
Francesco Fantin
VFV. D. Francesco
V. D. Francesco
GFGiorgia Fontana
Giorgia Fontana
AZAlessandra Zivelonghi
Alessandra Zivelonghi
LBLuisa Bissoli
Luisa Bissoli
MZMauro Zamboni
Mauro Zamboni
Background. Few studies have evaluated prospectively age-related body composition changes and their relationships with worsening disability in the elderly population. Methods. Ninety-seven women and 62 men aged 71.4 ± 2.2 and 71.6 ± 2.2 years, respectively, at baseline underwent dual-energy x-ray absorptiometry determinations at baseline and at 2- and 5.5-year follow-up intervals to measure total body and leg fat (FM) and total, appendicular, and leg fat-free mass (FFM). Height, weight, body mass index (BMI), and waist circumference (as well as reported disabilities using a four-level scale) were evaluated at baseline and at 2- and 5.5-year follow-up. Results. In both sexes, total FM did not change significantly, while total, appendicular, and leg FFM significantly decreased over the study follow-up. In men and women losing weight, BMI, total and leg FM, and total, appendicular, and leg FFM significantly decreased. In weight-stable men and women, appendicular and leg FFM significantly decreased and BMI, waist circumference, and total FM significantly increased. Men lost significantly more total, appendicular, and leg FFM than did women, irrespective of whether they maintained or lost weight. Over the follow-up period, 43.3% of women and 43.5% of men declined in one or more levels of reported disability. We evaluated the effect of age, baseline BMI, FM, FFM, number of diseases, baseline 6-minute walking test, categories of weight change, total, appendicular, or leg FFM changes, total FM and waist changes on the probability of a decline in one or more levels of reported disability score over the follow-up period, taking into account sex. Patients losing appendicular and leg FFM were 2.15 and 2.53 times, respectively, more likely to report increased disability than were patients without FFM loss. Conclusions. Reduction in appendicular or leg FFM was the main predictor of decline in one or more levels of reported disability in older men and women, and accounted for about a 2-fold increase in risk.