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Abstract Background Weight re-gain (which is also known as re-obesity) is an overwhelming challenge many dieters face in their pursuit to maintain consistent results following successful weight loss. This frustrating pattern of weight cycling can have various mental and physical implications, which further puts another roadblock in any weight reduction program. Main body of the abstract A comprehensive analysis of the causes behind the phenomenon of re-obesity has been widely conducted in literature, exploring the importance of creating the right mindset for weight loss maintenance and identifying the hormonal role, specifically of insulin–leptin resistance and ghrelin enhanced affinity, on appetite and food intake regulation. Insulin–Leptin resistance, due to circulating prostaglandins and prostaglandin metabolites, along with a decline in leptin-producing adipocytes following body mass reduction, cuts off leptin’s satiety signals to the brain. The persistence of this hormonal dysregulation after weight loss is collectively called obesogenic memory, and it seems to be largely mediated by dysbiosis. Short conclusion In conclusion, understanding of the influence of hormonal dysbiosis on re-obesity is fundamental in targeting the culprits behind ineffective attempts at weight loss sustenance, optimization of diet duration, use of synbiotics. Fecal and oral microbial transplantation hold high potential in improving long-term management interventions in obesity patients.

Introduction: Gestational vascular complications (GVCs), including gestational hypertension and preeclampsia, are leading causes of maternal morbidity and mortality. Elevated levels of extracellular vesicles (EVs), in GVC have been linked to vascular injury. This study aims to characterize placental and circulating EV miRNA in GVCs, and explores the involvement of EV-miRNA in GVC, and whether they may be used to distinguish between placental and maternal pathologies.Methods: Blood samples were obtained from 15 non-pregnant (NP), 18 healthy-pregnant (HP), and 23 women with GVC during the third trimester. Placental sections were obtained after caesarian section. Platelet-poor-plasma (PPP) and EV pellets were characterized: EV size/concentration, protein content and miRNA expression were measured by nanoparticle tracking analysis, western blot, nano-string technology and RT-PCR. The effects of EVs on trophoblasts and EC miRNA expression were evaluated.Results: Higher EVs concentrations were observed in HP-PPP and GVC-PPP (p < 0.0001) compared to the NP-PPP. The concentration of large EVs (>100 nm) was higher in PPP and EV pellets of HP and GVC compared to the NP group. EV pellets of pregnant women demonstrated lower expression of exosomal markers CD63/CD81 compared to NP-EVs. GVC-EVs expressed more human placental lactogen (hPL) hormone than HP-EVs, reflecting their placental origin. Screening of miRNAs in EV pellets and in PPP identified certain miRNAs that were highly expressed only in EVs pellets of the HP (13%) and GVC groups (15%), but not in the NP group. Differences were detected in the expression of hsa-miR-16-5p, hsa-miR-210, and hsa-miR-29b-3p. The expression of hsa-miR-16-5p and hsa-miR-210 was low in EV pellets obtained from NP, higher in HP-EVs, and significantly lower in GVC-EVs. Except for hsa-miR-29b-3p, which was upregulated in GVC, no significant differences were found in the levels of other miRNAs in placental sections. Exposure to GVC-EVs resulted in higher expression of hsa-miR-29b-3p compared to cells exposed to HP-EVs in villous trophoblasts, but not in EC.Conclusion: Expression of hsa-miR-16-5p and hsa-miR-210 reflects maternal pathophysiological status, while hsa-miR-29b-3p reflects placental status. These findings suggest that EV-miRNA are involved in GVC, and that they may be used to distinguish between pathologies of placental and maternal origins in preeclampsia.