Author: BalanceGenics Anti-aging Research Team (How100.com)
New Research Suggests Paternal Preconception Diet May Influence Offspring's Obesity Risk
It's so hard to lose weight. It is said that you should control eating habits and stay active. But have you ever thought that it's not enough to control eating habits, but you might have to cross over to pre-birth and control your dad’s eating habits?
A recent study published in Nature Communications suggests that when preparing for pregnancy, dads-to-be not only have to stop smoking and drinking, but also can't eat too much greasy food, which could affect their children's health and increase the risk of disease.
The study was led by a team of researchers from the University of Sydney, who used an innovative system of nutritional methods to systematically explore how adjusting the ratio of the three macronutrients (protein, fat, and carbohydrates) in a father's diet affects his offspring (both male and female offspring).
During the experiment, the researchers divided male mice into 10 groups, and each group was fed food with the same number of calories but varying proportions of macronutrients, such as a protein content varying between 10%-50%, a fat percentage of 10%-60%, and a carbohydrate percentage of 30%-70%. After 13 weeks on the specific diet, the male mice were mated with females who had been kept on a regular chow diet. And then the researchers conducted a thorough and detailed phenotypic characterization of their female offspring.
Image Figure 1: Effect of paternal diet on the metabolic phenotype of female offspring
The results of the study showed that female offspring of male mice consuming a high-fat diet were generally higher in body fat compared to offspring of other dietary groups. In particular, female offspring whose father's diet consisted of 45% fat, 34% carbohydrates, and 21% protein of calories exhibited the highest fasting blood glucose levels and accumulated the greatest amount of subcutaneous white fat.
In contrast, if the fathers consumed a high-protein, low-fat diet, their female offspring showed lower fasting blood glucose levels and less white fat accumulation. Even more critical is brown fat, which is relatively easy to burn for energy. In female offspring, however, the opposite trend in storage occurs: when their fathers consume a high-fat diet, these offspring instead have relatively low brown fat stores in their bodies.
These gender-specific impacts on metabolism and body composition are not manifested in the fathers themselves, suggesting that paternal dietary habits directly influence the intrinsic regulatory mechanisms during offspring development, rather than simply replicating the phenotypic traits of the fathers. The researchers hypothesize that epigenetic changes in the father's sperm may be one of the key mechanisms responsible for these paternal effects.
Certain dietary macronutrients are known to act on the genome to trigger changes in gene expression patterns that may be passed on to the next generation. For example, high fat intake may induce epigenetic modifications that make daughters more likely to increase fat storage and develop insulin resistance.
In fact, it's not just high-fat diets that can make offspring more likely to be obese, as can high blood sugar in fathers. In 2017, a Chinese research team from the Affiliated Hospital of Chongqing Medical University published their study in the Journal of Endocrinology.
In their study, they utilized male rats as subjects to simulate a hyperglycemic state by intraperitoneal injection of streptozotocin (STZ) or citrate buffer (CB). Subsequently, STZ-injected rats with blood glucose levels above a specific threshold were selected to mate with normal female rats to observe metabolic changes in their offspring.
The results of the study showed that the offspring from hyperglycemic fathers (STZ-O) exhibited different metabolic profiles from normal controls (CB-O) during their growth. Adult STZ-O weighed significantly more than CB-O, suggesting that offspring from hyperglycemic fathers may be more susceptible to obesity.
Further analysis revealed that STZ-O also performed worse in glucose and insulin tolerance tests, showing reduced insulin sensitivity. In addition, these rats had a significant increase in food intake when re-feeding after fasting, which further exacerbated their weight problems.
Similar to the study mentioned above, they also observed changes in the brown adipose tissue of STZ-O rats, with a downregulation of UCP1 levels. UCP1 is a factor associated with thermogenic activity, and its downregulation may lead to reduced energy expenditure, thereby increasing the risk of obesity.
More surprisingly, the study also found suppression of leptin signaling in the hypothalamus of STZ-O rats. Leptin is an important hormone that regulates appetite and energy balance. When leptin signaling is blocked, individuals may be more likely to feel hungry, leading to overeating and weight gain.
The researchers believe this same intergenerational transmission from epigenetic sources. As for the mechanism of transmission, previous studies have found that epigenetic changes can be transmitted through microRNAs in the father's sperm.
In a 2015 study published in the Proceedings of the National Academy of Sciences, scientists from the University of Pennsylvania created a model of paternal stress in which they found some specific microRNAs (miRs for short). When male mice were stressed, these miRs increased in their sperm. And, surprisingly, these increased miRs were associated with a diminished hypothalamic-pituitary-adrenal (or HPA) stress response in the offspring.
In the study, they further examined whether these sperm miRs affect the stress response of the offspring after fertilization and demonstrated a significant reproduction of the stress dysregulation phenotype in the offspring by injecting the fertilized eggs with these nine specific miRs. In addition the researchers found that these miRs may alter the transcriptome of the hypothalamus in the long term, leading to problems with HPA axis function. And the expression of extracellular matrix and collagen genes related to blood-brain barrier permeability was also decreased.
To gain more insight into the role of these miRs, the scientists also used a new technique to observe their effects in early fertilized eggs. It turned out that these miRs degrade some stored maternal mRNA transcripts, including the sirtuin 1 and ubiquitin-protein ligase E3a genes, which are involved in chromatin remodeling. This powerful regulatory function may have triggered a series of molecular events that ultimately altered the stress response of the offspring. This suggests that miRs in sperm play an important role in transmitting paternal experiences to offspring.
The epigenetic changes resulting from the poor dietary habits of fathers may also be transmitted to offspring in a similar manner. However, this requires further investigation. Thus, whether offspring become obese or not to a certain extent depends on their paternal inheritance. Only when prospective fathers maintain healthy dietary habits can their offspring be healthier.
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References
- Crean, A.J., Senior, A.M., Freire, T. et al. Paternal dietary macronutrient balance and energy intake drive metabolic and behavioral differences among offspring. Nat Commun (2024). https://doi.org/10.1038/s41467-024-46782-y
- Shi, X., Li, X., Hou, Y., Cao, X., Zhang, Y., Wang, H., Wang, H., Peng, C., Li, J., Li, Q., Wu, C., & Xiao, X. (2017). Paternal hyperglycemia in rats exacerbates the development of obesity in offspring. Journal of Endocrinology, 234(2), 175-186.
- Rodgers AB, Morgan CP, Leu NA, Bale TL. Transgenerational epigenetic programming via sperm microRNA recapitulates effects of paternal stress. Proc Natl Acad Sci U S A. 2015 Nov 3;112(44):13699-704. doi: 10.1073/pnas.1508347112. Epub 2015 Oct 19. PMID: 26483456; PMCID: PMC4640733.
