Paternal impact on the life course development of obesity and type 2 diabetes in the offspring

Abstract

The aetiologies of obesity and type 2 diabetes are incredibly complex, but the potential role of paternal influences remains relatively understudied. A better understanding of paternal influences on offspring risk of obesity and type 2 diabetes could have profound implications for public health, clinical practice and society. In this review, we outline potential biological and social mechanisms through which fathers might exert an impact on the health of their offspring. We also present a systematically compiled overview of the current evidence linking paternal factors to offspring development of obesity and type 2 diabetes throughout the life course. Although evidence is accumulating to support paternal associations with offspring outcomes, more high-quality research is needed to overcome specific methodological challenges and provide stronger causal evidence. Electronic supplementary material The online version of this article (10.1007/s00125-019-4919-9) contains peer-reviewed but unedited supplementary material including a slideset of the figures for download, which is available to authorised users.

Maternal but Not Paternal High-Fat Diet (HFD) Exposure at Conception Predisposes for ‘Diabesity’ in Offspring Generations

“…This contrasts with observations and wide reflections on epigenetic 'diabesity' transmission through the paternal line [13][14][15]. Similarly, in contrast to the aforementioned studies and a variety of rather narrative reviews [20,41,42], some other similar approaches also did not confirm respective 'diabesogenic' alterations in the paternal line F1 offspring after HFD exposure [35,43,44]. Accordingly, data and interpretations of paternal/epigenetic 'diabesity' transmission appear to remain inconclusive and need further distinct exploration, as provided here.…”

Western Diet Consumption During Development: Setting the Stage for Neurocognitive Dysfunction

“…The perinatal period in rodents, lasting from gestation to weaning (weaning at ∼postnatal day [PN] 21–24), is a time during which maternal exposures can have lasting effects on cognitive processes. Indeed, the perinatal developmental stage is a critical period for neuronal programming of regions involved in learning and memory, such as the medial prefrontal cortex (mPFC) and the hippocampus (HPC) ( Reynolds et al, 2017 ; Sharp and Lawlor, 2019 ). Although the exact timing varies slightly by strain, in rats PN 22–27 is considered the approximate juvenile stage of development, PN 28–42 equivalent to the early-mid adolescent period (∼12–17 years in humans), and PN 43–55 comparable to the late adolescence/emerging adulthood period in humans (∼18–25 years) ( Spear, 2016 ).…”

Molecular mechanisms governing offspring metabolic programming in rodent models of in utero stress

“…A significant paternal contribution to the developmental programming of offspring metabolism has recently come to light, with paternal exposure to alcohol or a high-fat or low-protein diet also programming adult offspring metabolism [257][258][259]. The mechanisms by which this occurs have been reviewed elsewhere [260][261][262][263][264] and above all highlight the need to also consider paternal environmental exposures when elucidating the mechanisms underlying the programming of metabolic disturbances in the offspring. Furthermore, the transmission of metabolic dysfunctions has been observed across subsequent generations even in the absence of further insults and normal environmental conditions via epigenetic processes (discussed previously; [265][266][267]).…”