PMID- 37355440
OWN - NLM
STAT- MEDLINE
DCOM- 20230925
LR  - 20231002
IS  - 1532-3102 (Electronic)
IS  - 0143-4004 (Linking)
VI  - 141
DP  - 2023 Sep 26
TI  - Paternal programming of fetoplacental and offspring metabolic disorders.
PG  - 71-77
LID - S0143-4004(23)00144-3 [pii]
LID - 10.1016/j.placenta.2023.06.009 [doi]
AB  - The alarming increase in the prevalence of metabolic pathologies is of worldwide 
      concern and has been linked not only to genetic factors but also to a large 
      number of non-genetic factors. In recent years, there has been increasing 
      interest in the study of the programming of metabolic diseases, such as type 2 
      diabetes mellitus (T2DM) and obesity, by paternal exposure, a paradigm termed 
      "Paternal Origins of Health and Disease" (POHaD). This term derives from the 
      better known "Developmental Origins of Health and Disease" (DOHaD), which focuses 
      on the involvement of the maternal intrauterine environment and complications 
      during pregnancy associated with the health and disease of the offspring. Studies 
      on paternal programming have documented environmentally induced epigenetic 
      modifications in the male germline and in seminal plasma, which lead to 
      intergenerational and transgenerational phenotypes, evident already during 
      fetoplacental development. Studies with animal models at both ends of the 
      nutritional spectrum (undernutrition or overnutrition) have been performed to 
      understand the possible mechanisms and signaling pathways leading to the 
      programming of metabolic disorders by exploring epigenetic changes throughout the 
      life of the offspring. The aim of this review was to address the evidence of the 
      programming of fetoplacental developmental alterations and metabolic pathologies 
      in the offspring of males with metabolic disorders and unhealthy exposures, 
      highlighting the mechanisms involved in such programming and looking for paternal 
      interventions to reduce negative health outcomes in the offspring.
CI  - Copyright (c) 2023 Elsevier Ltd. All rights reserved.
FAU - Capobianco, Evangelina
AU  - Capobianco E
AD  - Universidad de Buenos Aires, Facultad de Medicina, Buenos Aires, Argentina; 
      CONICET - Universidad de Buenos Aires, Laboratory of Reproduction and Metabolism, 
      CEFYBO, Buenos Aires, Argentina. Electronic address: evacapobianco@yahoo.com.ar.
FAU - Pirrone, Irune
AU  - Pirrone I
AD  - Universidad de Buenos Aires, Facultad de Medicina, Buenos Aires, Argentina; 
      CONICET - Universidad de Buenos Aires, Laboratory of Reproduction and Metabolism, 
      CEFYBO, Buenos Aires, Argentina.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20230618
PL  - Netherlands
TA  - Placenta
JT  - Placenta
JID - 8006349
SB  - IM
MH  - Pregnancy
MH  - Male
MH  - Humans
MH  - Animals
MH  - Female
MH  - *Diabetes Mellitus, Type 2/etiology
MH  - *Metabolic Diseases/genetics
MH  - Epigenesis, Genetic
MH  - Obesity/complications
MH  - Fathers
OTO - NOTNLM
OT  - Epigenetics
OT  - Fetal programming
OT  - Offspring
OT  - POHaD
OT  - Placenta
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/06/25 01:08
MHDA- 2023/09/25 06:43
CRDT- 2023/06/24 21:56
PHST- 2023/03/09 00:00 [received]
PHST- 2023/06/08 00:00 [revised]
PHST- 2023/06/11 00:00 [accepted]
PHST- 2023/09/25 06:43 [medline]
PHST- 2023/06/25 01:08 [pubmed]
PHST- 2023/06/24 21:56 [entrez]
AID - S0143-4004(23)00144-3 [pii]
AID - 10.1016/j.placenta.2023.06.009 [doi]
PST - ppublish
SO  - Placenta. 2023 Sep 26;141:71-77. doi: 10.1016/j.placenta.2023.06.009. Epub 2023 
      Jun 18.