Paternal low protein diet perturbs inter-generational metabolic homeostasis in a tissue-specific manner in mice.


Journal

Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179

Informations de publication

Date de publication:
08 09 2022
Historique:
received: 15 03 2022
accepted: 30 08 2022
entrez: 8 9 2022
pubmed: 9 9 2022
medline: 14 9 2022
Statut: epublish

Résumé

The underlying mechanisms driving paternally-programmed metabolic disease in offspring remain poorly defined. We fed male C57BL/6 mice either a control normal protein diet (NPD; 18% protein) or an isocaloric low protein diet (LPD; 9% protein) for a minimum of 8 weeks. Using artificial insemination, in combination with vasectomised male mating, we generated offspring using either NPD or LPD sperm but in the presence of NPD or LPD seminal plasma. Offspring from either LPD sperm or seminal fluid display elevated body weight and tissue dyslipidaemia from just 3 weeks of age. These changes become more pronounced in adulthood, occurring in conjunction with altered hepatic metabolic and inflammatory pathway gene expression. Second generation offspring also display differential tissue lipid abundance, with profiles similar to those of first generation adults. These findings demonstrate that offspring metabolic homeostasis is perturbed in response to a suboptimal paternal diet with the effects still evident within a second generation.

Identifiants

pubmed: 36075960
doi: 10.1038/s42003-022-03914-8
pii: 10.1038/s42003-022-03914-8
pmc: PMC9458637
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

929

Subventions

Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/R003556/1
Pays : United Kingdom
Organisme : Biotechnology and Biological Sciences Research Council
ID : BB/M027252/1
Pays : United Kingdom

Informations de copyright

© 2022. The Author(s).

Références

Fleming, T. P. et al. Origins of lifetime health around the time of conception: causes and consequences. Lancet 391, 1842–1852 (2018).
pubmed: 29673874 pmcid: 5975952 doi: 10.1016/S0140-6736(18)30312-X
Reynolds, C. M., Segovia, S. A. & Vickers, M. H. Experimental models of maternal obesity and neuroendocrine programming of metabolic disorders in offspring. Front. Endocrinol. (Lausanne) 8, 245 (2017).
doi: 10.3389/fendo.2017.00245
Alwasel, S. H. et al. Intergenerational effects of in utero exposure to Ramadan in Tunisia. Am. J. Hum. Biol. 25, 341–343 (2013).
pubmed: 23436278 doi: 10.1002/ajhb.22374
Painter, R. C. et al. Transgenerational effects of prenatal exposure to the Dutch famine on neonatal adiposity and health in later life. BJOG 115, 1243–1249 (2008).
pubmed: 18715409 doi: 10.1111/j.1471-0528.2008.01822.x
Pentinat, T., Ramon-Krauel, M., Cebria, J., Diaz, R. & Jimenez-Chillaron, J. C. Transgenerational inheritance of glucose intolerance in a mouse model of neonatal overnutrition. Endocrinology 151, 5617–5623 (2010).
pubmed: 20943806 doi: 10.1210/en.2010-0684
Saben, J. L. et al. Maternal metabolic syndrome programs mitochondrial dysfunction via germline changes across three generations. Cell Rep. 16, 1–8 (2016).
pubmed: 27320925 pmcid: 4957639 doi: 10.1016/j.celrep.2016.05.065
Su, L. & Patti, M. E. Paternal nongenetic intergenerational transmission of metabolic disease risk. Curr. Diab. Rep. 19, 38 (2019).
pubmed: 31127415 doi: 10.1007/s11892-019-1163-0
Morgan, H. L. & Watkins, A. J. The influence of seminal plasma on offspring development and health. Semin. Cell Dev. Biol. 97, 131–137 (2020).
pubmed: 31254609 doi: 10.1016/j.semcdb.2019.06.008
Donkin, I. & Barres, R. Sperm epigenetics and influence of environmental factors. Mol. Metab. 14, 1–11 (2018).
pubmed: 29525406 pmcid: 6034033 doi: 10.1016/j.molmet.2018.02.006
Zheng, X. et al. Sperm epigenetic alterations contribute to inter- and transgenerational effects of paternal exposure to long-term psychological stress via evading offspring embryonic reprogramming. Cell Discov. 7, 101 (2021).
pubmed: 34711814 pmcid: 8553786 doi: 10.1038/s41421-021-00343-5
Schjenken, J. E. & Robertson, S. A. The female response to seminal fluid. Physiol. Rev. 100, 1077–1117 (2020).
pubmed: 31999507 doi: 10.1152/physrev.00013.2018
Furse, S. et al. Lipid Traffic Analysis reveals the impact of high paternal carbohydrate intake on offsprings’ lipid metabolism. Commun. Biol. 4, 163 (2021).
pubmed: 33547386 pmcid: 7864968 doi: 10.1038/s42003-021-01686-1
Watkins, A. J. et al. Paternal diet programs offspring health through sperm- and seminal plasma-specific pathways in mice. Proc. Natl Acad. Sci. USA 115, 10064–10069 (2018).
pubmed: 30150380 pmcid: 6176621 doi: 10.1073/pnas.1806333115
Morgan, H. L. et al. Paternal diet impairs F1 and F2 offspring vascular function through sperm and seminal plasma specific mechanisms in mice. J. Physiol. 598, 699–715 (2020).
pubmed: 31617219 doi: 10.1113/JP278270
Sovaila, S., Purcarea, A., Gheonea, D., Ionescu, S. & Ciurea, T. Cellular interactions in the human fatty liver. J. Med. Life 12, 338–340 (2019).
pubmed: 32025251 pmcid: 6993300 doi: 10.25122/jml-2019-1010
Pei, K. et al. An overview of lipid metabolism and nonalcoholic fatty liver disease. BioMed. Res. Int. 2020, 4020249 (2020).
pubmed: 32733940 pmcid: 7383338 doi: 10.1155/2020/4020249
Li, Z., Berk, M., McIntyre, T. M., Gores, G. J. & Feldstein, A. E. The lysosomal-mitochondrial axis in free fatty acid-induced hepatic lipotoxicity. Hepatology 47, 1495–1503 (2008).
pubmed: 18220271 doi: 10.1002/hep.22183
Suganami, T., Tanaka, M. & Ogawa, Y. Adipose tissue inflammation and ectopic lipid accumulation. Endocr. J. 59, 849–857 (2012).
pubmed: 22878669 doi: 10.1507/endocrj.EJ12-0271
Allison, S. J. Fibrosis: dysfunctional fatty acid oxidation in renal fibrosis. Nat. Rev. Nephrol. 11, 64 (2015).
pubmed: 25536395 doi: 10.1038/nrneph.2014.244
Han, Y. et al. Lipophagy deficiency exacerbates ectopic lipid accumulation and tubular cells injury in diabetic nephropathy. Cell Death Dis. 12, 1031 (2021).
pubmed: 34718329 pmcid: 8557213 doi: 10.1038/s41419-021-04326-y
Chiurchiu, V., Leuti, A., Smoum, R., Mechoulam, R. & Maccarrone, M. Bioactive lipids ALIAmides differentially modulate inflammatory responses of distinct subsets of primary human T lymphocytes. FASEB J. 32, 5716–5723 (2018).
pubmed: 29879374 doi: 10.1096/fj.201800107R
Xia, J. Y., Morley, T. S. & Scherer, P. E. The adipokine/ceramide axis: key aspects of insulin sensitization. Biochimie 96, 130–139 (2014).
pubmed: 23969158 doi: 10.1016/j.biochi.2013.08.013
Schoeler, M. & Caesar, R. Dietary lipids, gut microbiota and lipid metabolism. Rev. Endocr. Metab. Disord. 20, 461–472 (2019).
pubmed: 31707624 pmcid: 6938793 doi: 10.1007/s11154-019-09512-0
Caesar, R., Tremaroli, V., Kovatcheva-Datchary, P., Cani, P. D. & Backhed, F. Crosstalk between gut microbiota and dietary lipids aggravates WAT inflammation through TLR signaling. Cell Metab. 22, 658–668 (2015).
pubmed: 26321659 pmcid: 4598654 doi: 10.1016/j.cmet.2015.07.026
Kindt, A. et al. The gut microbiota promotes hepatic fatty acid desaturation and elongation in mice. Nat. Commun. 9, 3760 (2018).
pubmed: 30218046 pmcid: 6138742 doi: 10.1038/s41467-018-05767-4
Cropley, J. E. et al. Male-lineage transmission of an acquired metabolic phenotype induced by grand-paternal obesity. Mol. Metab. 5, 699–708 (2016).
pubmed: 27656407 pmcid: 5021672 doi: 10.1016/j.molmet.2016.06.008
Pembrey, M. E. et al. Sex-specific, male-line transgenerational responses in humans. Eur. J. Hum. Genet. 14, 159–166 (2006).
pubmed: 16391557 doi: 10.1038/sj.ejhg.5201538
Amati, F. et al. Skeletal muscle triglycerides, diacylglycerols, and ceramides in insulin resistance: another paradox in endurance-trained athletes? Diabetes 60, 2588–2597 (2011).
pubmed: 21873552 pmcid: 3178290 doi: 10.2337/db10-1221
Kang, S. C., Kim, B. R., Lee, S. Y. & Park, T. S. Sphingolipid metabolism and obesity-induced inflammation. Front. Endocrinol. (Lausanne) 4, 67 (2013).
doi: 10.3389/fendo.2013.00067
Holland, W. L. et al. Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid-induced ceramide biosynthesis in mice. J. Clin. Investig. 121, 1858–1870 (2011).
pubmed: 21490391 pmcid: 3083776 doi: 10.1172/JCI43378
Kolak, M. et al. Adipose tissue inflammation and increased ceramide content characterize subjects with high liver fat content independent of obesity. Diabetes 56, 1960–1968 (2007).
pubmed: 17620421 doi: 10.2337/db07-0111
Li, Z. et al. The ratio of phosphatidylcholine to phosphatidylethanolamine influences membrane integrity and steatohepatitis. Cell Metab. 3, 321–331 (2006).
pubmed: 16679290 doi: 10.1016/j.cmet.2006.03.007
van der Veen, J. N. et al. The critical role of phosphatidylcholine and phosphatidylethanolamine metabolism in health and disease. Biochim. Biophys. Acta Biomembr. 1859, 1558–1572 (2017).
pubmed: 28411170 doi: 10.1016/j.bbamem.2017.04.006
Jornayvaz, F. R. et al. Hepatic insulin resistance in mice with hepatic overexpression of diacylglycerol acyltransferase 2. Proc. Natl Acad. Sci. USA 108, 5748–5752 (2011).
pubmed: 21436037 pmcid: 3078388 doi: 10.1073/pnas.1103451108
Yang, Z. H., Miyahara, H., Takeo, J. & Katayama, M. Diet high in fat and sucrose induces rapid onset of obesity-related metabolic syndrome partly through rapid response of genes involved in lipogenesis, insulin signalling and inflammation in mice. Diabetol. Metab. Syndr. 4, 32 (2012).
pubmed: 22762794 pmcid: 3407732 doi: 10.1186/1758-5996-4-32
Longo, M. et al. Adipose tissue dysfunction as determinant of obesity-associated metabolic complications. Int. J. Mol. Sci. https://doi.org/10.3390/ijms20092358 (2019).
Rhee, E. P. et al. Lipid profiling identifies a triacylglycerol signature of insulin resistance and improves diabetes prediction in humans. J. Clin. Investig. 121, 1402–1411 (2011).
pubmed: 21403394 pmcid: 3069773 doi: 10.1172/JCI44442
Agbaga, M. P., Mandal, M. N. & Anderson, R. E. Retinal very long-chain PUFAs: new insights from studies on ELOVL4 protein. J. lipid Res. 51, 1624–1642 (2010).
pubmed: 20299492 pmcid: 2882734 doi: 10.1194/jlr.R005025
Forouhi, N. G. et al. Differences in the prospective association between individual plasma phospholipid saturated fatty acids and incident type 2 diabetes: the EPIC-InterAct case-cohort study. Lancet Diabetes Endocrinol. 2, 810–818 (2014).
pubmed: 25107467 pmcid: 4196248 doi: 10.1016/S2213-8587(14)70146-9
Malik, V. S. et al. Circulating very-long-chain saturated fatty acids and incident coronary heart disease in US men and women. Circulation 132, 260–268 (2015).
pubmed: 26048094 pmcid: 4519378 doi: 10.1161/CIRCULATIONAHA.114.014911
Wiesner, P., Leidl, K., Boettcher, A., Schmitz, G. & Liebisch, G. Lipid profiling of FPLC-separated lipoprotein fractions by electrospray ionization tandem mass spectrometry. J. Lipid Res. 50, 574–585 (2009).
pubmed: 18832345 doi: 10.1194/jlr.D800028-JLR200
Furse, S. & de Kroon, A. I. Phosphatidylcholine’s functions beyond that of a membrane brick. Mol. Membr. Biol. 32, 117–119 (2015).
pubmed: 26306852 doi: 10.3109/09687688.2015.1066894
Machado, M. V. et al. How adiponectin, leptin, and ghrelin orchestrate together and correlate with the severity of nonalcoholic fatty liver disease. Eur. J. Gastroenterol. Hepatol. 24, 1166–1172 (2012).
pubmed: 22735605 doi: 10.1097/MEG.0b013e32835609b0
Hossain, I. A., Akter, S., Rahman, M. K. & Ali, L. Gender specific association of serum leptin and insulinemic indices with nonalcoholic fatty liver disease in prediabetic subjects. PLoS ONE 10, e0142165 (2015).
pubmed: 26569494 pmcid: 4646431 doi: 10.1371/journal.pone.0142165
Lambert, J. E., Ramos-Roman, M. A., Browning, J. D. & Parks, E. J. Increased de novo lipogenesis is a distinct characteristic of individuals with nonalcoholic fatty liver disease. Gastroenterology 146, 726–735 (2014).
pubmed: 24316260 doi: 10.1053/j.gastro.2013.11.049
Fullerton, M. D. et al. Single phosphorylation sites in Acc1 and Acc2 regulate lipid homeostasis and the insulin-sensitizing effects of metformin. Nat. Med. 19, 1649–1654 (2013).
pubmed: 24185692 pmcid: 4965268 doi: 10.1038/nm.3372
Simopoulos, C. et al. Neuropeptide urocortin 1 and its receptors are expressed in the human liver. Neuroendocrinology 89, 315–326 (2009).
pubmed: 19096201 doi: 10.1159/000187136
Le Chatelier, E. et al. Richness of human gut microbiome correlates with metabolic markers. Nature 500, 541–546 (2013).
pubmed: 23985870 doi: 10.1038/nature12506
Karlsson, F. H. et al. Gut metagenome in European women with normal, impaired and diabetic glucose control. Nature 498, 99–103 (2013).
pubmed: 23719380 doi: 10.1038/nature12198
Karlsson, F. H. et al. Symptomatic atherosclerosis is associated with an altered gut metagenome. Nat. Commun. 3, 1245 (2012).
pubmed: 23212374 doi: 10.1038/ncomms2266
Wargent, E. et al. Prolonged treatment of genetically obese mice with conjugated linoleic acid improves glucose tolerance and lowers plasma insulin concentration: possible involvement of PPAR activation. Lipids Health Dis. 4, 3 (2005).
pubmed: 15642120 pmcid: 546236 doi: 10.1186/1476-511X-4-3
Chen, P. et al. Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice. Gastroenterology 148, 203–214.e216 (2015).
pubmed: 25239591 doi: 10.1053/j.gastro.2014.09.014
Le Blevec, E., Muronova, J., Ray, P. F. & Arnoult, C. Paternal epigenetics: mammalian sperm provide much more than DNA at fertilization. Mol. Cell. Endocrinol. 518, 110964 (2020).
pubmed: 32738444 doi: 10.1016/j.mce.2020.110964
Lee, S. et al. Skeletal muscle phosphatidylcholine and phosphatidylethanolamine respond to exercise and influence insulin sensitivity in men. Sci. Rep. 8, 6531 (2018).
pubmed: 29695812 pmcid: 5916947 doi: 10.1038/s41598-018-24976-x
Tasseva, G. et al. Phosphatidylethanolamine deficiency in Mammalian mitochondria impairs oxidative phosphorylation and alters mitochondrial morphology. J. Biol. Chem. 288, 4158–4173 (2013).
pubmed: 23250747 doi: 10.1074/jbc.M112.434183
Carone, B. R. et al. Paternally induced transgenerational environmental reprogramming of metabolic gene expression in mammals. Cell 143, 1084–1096 (2010).
pubmed: 21183072 pmcid: 3039484 doi: 10.1016/j.cell.2010.12.008
Chen, Q. et al. Sperm tsRNAs contribute to intergenerational inheritance of an acquired metabolic disorder. Science 351, 397–400 (2016).
pubmed: 26721680 doi: 10.1126/science.aad7977
Bromfield, J. J. et al. Maternal tract factors contribute to paternal seminal fluid impact on metabolic phenotype in offspring. Proc. Natl Acad. Sci. USA 111, 2200–2205 (2014).
pubmed: 24469827 pmcid: 3926084 doi: 10.1073/pnas.1305609111
Allen, C. P., Marconi, N., McLernon, D. J., Bhattacharya, S. & Maheshwari, A. Outcomes of pregnancies using donor sperm compared with those using partner sperm: systematic review and meta-analysis. Hum. Reprod. Update https://doi.org/10.1093/humupd/dmaa030 (2020).
Wang, J. X. et al. Surgically obtained sperm, and risk of gestational hypertension and pre-eclampsia. Lancet 359, 673–674 (2002).
pubmed: 11879865 doi: 10.1016/S0140-6736(02)07804-2
Carty, J. L. et al. The effects of vitamin C supplementation on protein oxidation in healthy volunteers. Biochem. Biophys. Res. Commun. 273, 729–735 (2000).
pubmed: 10873672 doi: 10.1006/bbrc.2000.3014
Furse, S. et al. A high throughput platform for detailed lipidomic analysis of a range of mouse and human tissues. Anal. Bioanal. Chem. 412, 2851–2862 (2020).
pubmed: 32144454 pmcid: 7196091 doi: 10.1007/s00216-020-02511-0
Furse, S. et al. A high-throughput platform for detailed lipidomic analysis of a range of mouse and human tissues. Anal. Bioanal. Chem. 412, 2851–2862 (2020).
pubmed: 32144454 pmcid: 7196091 doi: 10.1007/s00216-020-02511-0
Furse, S. & Koulman, A. The lipid and glyceride profiles of infant formula differ by manufacturer, region and date sold. Nutrients https://doi.org/10.3390/nu11051122 (2019).
Harshfield, E. L. et al. An unbiased lipid phenotyping approach to study the genetic determinants of lipids and their association with coronary heart disease risk factors. J. Proteome Res. 18, 2397–2410 (2019).
pubmed: 30887811 pmcid: 6558644 doi: 10.1021/acs.jproteome.8b00786
Caporaso, J. G. et al. QIIME allows analysis of high-throughput community sequencing data. Nat. Methods 7, 335–336 (2010).
pubmed: 20383131 pmcid: 3156573 doi: 10.1038/nmeth.f.303

Auteurs

Hannah L Morgan (HL)

Lifespan and Population Health, School of Medicine, University of Nottingham, Nottingham, NG7 2UH, UK.

Samuel Furse (S)

Core Metabolomics and Lipidomics Laboratory, Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Addenbrooke's Treatment Centre, Keith Day Road, Cambridge, CB2 0QQ, UK.
Wellcome-MRC Institute of Metabolic Science and Medical Research Council Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 0QQ, UK.
Biological Chemistry Group, Jodrell Laboratory, Royal Botanic Gardens Kew, Richmond, TW9 3AE, UK.

Irundika H K Dias (IHK)

Aston Medical School, Aston University, Aston Triangle, Birmingham, B4 7ET, UK.

Kiran Shabir (K)

Aston Medical School, Aston University, Aston Triangle, Birmingham, B4 7ET, UK.

Marcos Castellanos (M)

Nottingham Arabidopsis Stock Centre (NASC), University of Nottingham, Sutton Bonington Campus, Plant Science Building, School of Biosciences, Loughborough, LE12 5RD, UK.

Iqbal Khan (I)

Nottingham Arabidopsis Stock Centre (NASC), University of Nottingham, Sutton Bonington Campus, Plant Science Building, School of Biosciences, Loughborough, LE12 5RD, UK.

Sean T May (ST)

Nottingham Arabidopsis Stock Centre (NASC), University of Nottingham, Sutton Bonington Campus, Plant Science Building, School of Biosciences, Loughborough, LE12 5RD, UK.

Nadine Holmes (N)

Deep Seq, School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.

Matthew Carlile (M)

Deep Seq, School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.

Fei Sang (F)

Deep Seq, School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.

Victoria Wright (V)

Deep Seq, School of Life Sciences, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.

Albert Koulman (A)

Core Metabolomics and Lipidomics Laboratory, Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Addenbrooke's Treatment Centre, Keith Day Road, Cambridge, CB2 0QQ, UK.
Wellcome-MRC Institute of Metabolic Science and Medical Research Council Metabolic Diseases Unit, University of Cambridge, Cambridge, CB2 0QQ, UK.

Adam J Watkins (AJ)

Lifespan and Population Health, School of Medicine, University of Nottingham, Nottingham, NG7 2UH, UK. adam.watkins@nottingham.ac.uk.

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