title: Excess pregnancy weight gain leads to early indications of metabolic syndrome in a swine model of fetal programming.
abstract: Few data exist on the impact of maternal weight gain on offspring despite evidence demonstrating that early-life environment precipitates risks for metabolic syndrome. We hypothesized that excessive weight gain during pregnancy results in programming that predisposes offspring to obesity and metabolic syndrome. We further hypothesized that early postweaning nutrition alters the effects of maternal weight gain on indications of metabolic syndrome in offspring. Pregnant sows and their offspring were used for these experiments due to similarities with human digestive physiology, metabolism, and neonatal development. First parity sows fed a high-energy (maternal nutrition high energy [MatHE]) diet gained 12.4 kg (42%) more weight during pregnancy than sows fed a normal energy (maternal nutrition normal energy) diet. Birth weight and litter characteristics did not differ, but offspring MatHE gilts weighed more (P < .05) at age of 3 weeks (4.35 vs 5.24 ± 0.35 kg). At age of 12 weeks, offspring from MatHE mothers that were weaned onto a high-energy diet had elevated (P < .05) blood glucose (102 vs 64 mg/dL, confidence interval [CI]: 67-91), insulin (0.21 vs 0.10 ng/mL, CI: 0.011-0.019), and lower nonesterified fatty acid (0.31 vs 0.62 mmol/L, CI: 0.34-0.56) than offspring from the same MatHE sows weaned to the normal energy diet. These effects were not observed for offspring from sows fed a normal energy diet during pregnancy. These data indicate that excessive gestational weight gain during pregnancy in a pig model promotes early indications of metabolic syndrome in offspring that are further promoted by a high-energy postweaning diet.
authors.affiliation: The University of Texas Medical Branch at Galveston, Galveston 77555-0144 TX.
authors.forename: Emily J
authors.initials: EJ
authors.lastname: Arentson-Lantz
authors.affiliation: Department of Nutrition Science, Purdue University, Lafayette, IN.
authors.forename: Kimberly K
authors.initials: KK
authors.lastname: Buhman
authors.affiliation: Interdepartmental Nutrition Program, Purdue University, Lafayette, IN; Department of Animal Sciences, Purdue University, Lafayette, IN.
authors.forename: Kolapo
authors.initials: K
authors.lastname: Ajuwon
authors.affiliation: Interdepartmental Nutrition Program, Purdue University, Lafayette, IN; Department of Animal Sciences, Purdue University, Lafayette, IN. Electronic address: sdonkin@purdue.edu.
authors.forename: Shawn S
authors.initials: SS
authors.lastname: Donkin
mesh_terms: D050154:Adiposity / Q000502:physiology; D000818:Animals; D001724:Birth Weight; D001786:Blood Glucose / Q000378:metabolism; D004032:Diet / Q000662:veterinary; D004195:Disease Models, Animal; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D007328:Insulin / Q000097:blood; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D024821:Metabolic Syndrome / Q000378:metabolism; D009752:Nutritional Status; D009765:Obesity / Q000378:metabolism; D010729:Phosphoenolpyruvate Carboxykinase (GTP) / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013552:Swine; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014886:Weaning; D015430:Weight Gain / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D012333:RNA, Messenger; D014157:Transcription Factors; D010729:Phosphoenolpyruvate Carboxykinase (GTP)
keywords: Insulin resistance; Maternal weight gain; Metabolic syndrome; Pig; Programming