PMID- 31347485 OWN - NLM STAT- MEDLINE DCOM- 20200629 LR - 20200629 IS - 2040-1752 (Electronic) IS - 2040-1744 (Linking) VI - 10 IP - 4 DP - 2019 Aug TI - Maternal undernutrition results in altered renal pro-inflammatory gene expression concomitant with hypertension in adult male offspring that is ameliorated following pre-weaning growth hormone treatment. PG - 459-468 LID - 10.1017/S2040174418000922 [doi] AB - An adverse early life environment is associated with increased cardiovascular disease in offspring. Work in animal models has shown that maternal undernutrition (UN) during pregnancy leads to hypertension in adult offspring, with effects thought to be mediated in part via altered renal function. We have previously shown that growth hormone (GH) treatment of UN offspring during the pre-weaning period can prevent the later development of cardiometabolic disorders. However, the mechanistic basis for these observations is not well defined. The present study examined the impact of GH treatment on renal inflammatory markers in adult male offspring as a potential mediator of these reversal effects. Female Sprague-Dawley rats were fed either a chow diet fed ad libitum (CON) or at 50% of CON intake (UN) during pregnancy. All dams were fed the chow diet ad libitum during lactation. CON and UN pups received saline (CON-S/UN-S) or GH (2.5 microg/g/day; CON-GH/UN-GH) from postnatal day 3 until weaning (p21). Post-weaning males were fed a standard chow diet for the remainder of the study (150 days). Histological analysis was performed to examine renal morphological characteristics, and gene expression of inflammatory and vascular markers were assessed. There was evidence of renal hypotrophy and reduced nephron number in the UN-S group. Tumour necrosis factor-alpha, monocyte chemoattractant protein-1 (MCP-1), intercellular adhesion molecular-1 and vascular cell adhesion molecule-1 gene expression was increased in UN-S offspring and normalized in the UN-GH group. These findings indicate that pre-weaning GH treatment has the potential to normalize some of the adverse renal and cardiovascular sequelae that arise as a consequence of poor maternal nutrition. FAU - Zhang, X D AU - Zhang XD AD - Liggins Institute, University of Auckland,Auckland,New Zealand. FAU - Reynolds, C M AU - Reynolds CM AD - Liggins Institute, University of Auckland,Auckland,New Zealand. FAU - Gray, C AU - Gray C AD - Liggins Institute, University of Auckland,Auckland,New Zealand. FAU - Li, M AU - Li M AD - Liggins Institute, University of Auckland,Auckland,New Zealand. FAU - Vickers, M H AU - Vickers MH AD - Liggins Institute, University of Auckland,Auckland,New Zealand. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - J Dev Orig Health Dis JT - Journal of developmental origins of health and disease JID - 101517692 RN - 0 (Inflammation Mediators) RN - 9002-72-6 (Growth Hormone) SB - IM MH - Animals MH - Female MH - Gene Expression Regulation/*drug effects MH - Growth Hormone/*administration & dosage MH - Hypertension/*drug therapy/etiology MH - Inflammation/*drug therapy/etiology/metabolism MH - Inflammation Mediators/*metabolism MH - Kidney/*drug effects/immunology/pathology MH - Male MH - Malnutrition/*complications MH - Pregnancy MH - Rats MH - Rats, Sprague-Dawley MH - Weaning OTO - NOTNLM OT - renal inflammation OT - cardiovascular disease OT - developmental programming OT - hypertension OT - maternal undernutrition EDAT- 2019/07/28 06:00 MHDA- 2020/07/01 06:00 CRDT- 2019/07/27 06:00 PHST- 2019/07/27 06:00 [entrez] PHST- 2019/07/28 06:00 [pubmed] PHST- 2020/07/01 06:00 [medline] AID - S2040174418000922 [pii] AID - 10.1017/S2040174418000922 [doi] PST - ppublish SO - J Dev Orig Health Dis. 2019 Aug;10(4):459-468. doi: 10.1017/S2040174418000922.