Sexual dimorphic evolution of metabolic programming in non-genetic non-alimentary mild metabolic syndrome model in mice depends on feed-back mechanisms integrity for pro-opiomelanocortin-derived endogenous substances

Loizzo, Stefano; Vella, Stefano; Loizzo, Alberto; Fortuna, Andrea; Biase, Antonella Di; Salvati, Serafina; Frajese, Giovanni Vanni; Agrapart, Vincent; Morales, Rafael; Spampinato, Santi; Campana, Gabriele; Capasso, Anna; Galietta, Gabriella; Gracia-Rubio, Irene; Carta, Stefania; Carru, Ciriaco; Zinellu, Angelo; Ghirlanda, Giovanni; Seghieri, Giuseppe; Renzi, Paolo; Franconi, Flavia

doi:10.1016/j.peptides.2010.05.006

Cited by 12 publications

(25 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cortisol is metabolized reversibly by 11βHSD2, and irreversibly by α- and β-ring reductases and CYP3A. Animal studies showed a lower bioavailability of glucocorticoids in females due to decreased 11βHSD1 [16–18] and relatively increased 11βHSD2 activity [18], as compared to males. In addition, previous observations in humans suggest that estrogens could alter hepatic cortisol metabolism through increased CYP3A activity [19, 20] and decreased A-ring reduction [3, 21].…”

Section: Discussionmentioning

confidence: 99%

Gender-specific differences in hypothalamus–pituitary–adrenal axis activity during childhood: a systematic review and meta-analysis

et al. 2017

View full text Add to dashboard Cite

BackgroundGender-specific differences in hypothalamus–pituitary–adrenal (HPA) axis activity have been postulated to emerge during puberty. We conducted a systematic review and meta-analysis to test the hypothesis that gender-specific differences in HPA axis activity are already present in childhood.MethodsFrom inception to January 2016, PubMed and EMBASE.com were searched for studies that assessed non-stimulated cortisol in serum or saliva or cortisol in 24-h urine in healthy males and females aged ≤18 years. Studies that conform with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) statement were reported. Standardized mean differences (95% CIs) were calculated and analyzed using fixed-effect meta-analysis stratified for age: <8 years (prepubertal) and 8–18 years (peri-/postpubertal). For comparison, we ran the same analyses using random-effects models.ResultsTwo independent assessors selected 413 out of 6158 records (7%) for full-text screening, of which 79 articles were included. Of these, 58 (with data on 16,551 subjects) were included in the meta-analysis. Gender differences in cortisol metabolism differed per age group. Boys aged <8 years had 0.18 (0.06; 0.30) nmol/L higher serum and 0.21 (0.05; 0.37) nmol/L higher salivary cortisol levels, while between 8 and 18 years, boys had 0.34 (0.28; 0.40) nmol/L lower serum and 0.42 (0.38; 0.47) nmol/L lower salivary cortisol levels. In 24-h urine, cortisol was consistently higher in boys, being 0.34 (0.05; 0.64) and 0.32 (0.17; 0.47) μg/24 h higher in the <8- and 8–18-year groups, respectively. However, gender-differences in serum cortisol <8 years and between 8 and 18 years were absent when using random-effects models.ConclusionsGender differences in cortisol metabolism are already present in childhood, with higher salivary cortisol in boys aged <8 years compared to girls. This pattern was reversed after the age of 8 years. In contrast, the gender-specific difference in cortisol production as assessed through 24-h urine did not change with age. Although differences were small, and analyses of gender differences in serum cortisol were inconclusive, they might contribute to gender-specific origins of health and disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s13293-016-0123-5) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Gender-specific differences in hypothalamus–pituitary–adrenal axis activity during childhood: a systematic review and meta-analysis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…However, for the first time we could demonstrate the importance of either systems for the triggering of various specific signs and symptoms of an experimental type-2 diabetes model (Loizzo et al 2012). Much work should be performed to better understand the molecular bases of the previously described mechanisms involved in diabetes model pathogenesis, which are at least in part gender dependent (Loizzo et al 2010c); the involvement of other hormonal-neurohumoral systems (e.g. adrenergic) should also be considered.…”

Section: Enduring Improved Efficiency Of the Cns And The Visual Systemmentioning

confidence: 93%

Enhanced brain performance in mice following postnatal stress

Loizzo

Spampinato

Campana

et al. 2012

Journal of Endocrinology

Self Cite

View full text Add to dashboard Cite

The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic-functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid-and/or ACTH-corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologicneurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with 'classic' diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic-neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (Kw8%); increased level (Cw40%) and reduced latency (Kw30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (Cw135% latency); and enhanced brain-derived neurotrophic factor level (Cw70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTHcorticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic-neurophysiologic performances. Taken all together, these findings are compatible with an 'enduring acute-stress' reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal-metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.

show abstract

“…There are some data that nutritional intervention can prevent metabolic alteration induced by environmental changes during the lactation period. In fact, metabolic alterations induced by psychological distress (maternal separation) and painful stimulus during lactation produces permanent metabolic alteration (overweight, increase in plasma lipids and fasting glucose) in male mice (Loizzo et al, 2006;Loizzo et al, 2010). The metabolic alterations are related to alterations in the hypothalamus-pituitary adrenal axis (Loizzo et al, 2010) and can be prevented by taurine (Loizzo et al, 2007).…”

Section: Early Events and Developmental Plasticitymentioning

confidence: 99%

“…In fact, metabolic alterations induced by psychological distress (maternal separation) and painful stimulus during lactation produces permanent metabolic alteration (overweight, increase in plasma lipids and fasting glucose) in male mice (Loizzo et al, 2006;Loizzo et al, 2010). The metabolic alterations are related to alterations in the hypothalamus-pituitary adrenal axis (Loizzo et al, 2010) and can be prevented by taurine (Loizzo et al, 2007). Taurine is a sulfur semi-essential amino acid and is added to many milk formulas; taurine plays a role in glucose metabolism (Franconi et al, 2004;Franconi et al, 2006b), especially during early life (Aerts and Van Assche, 2002;Cherif et al, 1998;Dahri et al, 1991).…”

Section: Early Events and Developmental Plasticitymentioning

confidence: 99%