title: High-fat/fructose feeding during prenatal and postnatal development in female rats increases susceptibility to renal and metabolic injury later in life.
abstract: Accumulating evidence suggests that both an adverse prenatal and early postnatal environment increase susceptibility to renal and metabolic dysfunction later in life; however, whether exposure to adverse conditions during both prenatal and postnatal development act synergistically to potentiate the severity of renal and metabolic injury remains unknown. Sprague-Dawley rats were fed either a standard diet or a diet high in fat/fructose throughout pregnancy and lactation. After being weaned, female offspring were randomized to either standard diet or the high-fat/high-fructose diet, resulting in the following treatment groups: NF-NF, offspring of mothers fed a standard diet and fed a standard diet postnatally; NF-HF, offspring of mothers fed a standard diet and fed a high-fat/fructose diet postnatally; HF-NF, offspring of mothers fed a high-fat/fructose diet and fed a standard diet postnatally; HF-HF, offspring of mothers fed a high-fat/fructose diet and fed a high-fat/fructose diet postnatally. At the time of euthanasia (17 wk of age), HF-HF offspring weighed 30% more and had 110% more visceral fat than NF-NF offspring. The HF-HF offspring also had elevated blood glucose levels, glucose intolerance, 286% increase in urine albumin excretion, and 60% increase in glomerulosclerosis compared with NF-NF. In addition, HF-HF offspring exhibited a 100% increase in transforming growth factor-β protein expression and 116% increase in the abundance of infiltrated macrophages compared with the NF-NF offspring. These observations suggest that high-fat/fructose feeding during prenatal and throughout postnatal life increases the susceptibility to renal and metabolic injury later in life.
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA.
authors.forename: Elizabeth R
authors.initials: ER
authors.lastname: Flynn
authors.forename: Barbara T
authors.initials: BT
authors.lastname: Alexander
authors.forename: Jonathan
authors.initials: J
authors.lastname: Lee
authors.forename: Zachary M
authors.initials: ZM
authors.lastname: Hutchens
authors.forename: Christine
authors.initials: C
authors.lastname: Maric-Bilkan
mesh_terms: D000419:Albuminuria / Q000097:blood / Q000209:etiology / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D059305:Diet, High-Fat / Q000009:adverse effects*; D004198:Disease Susceptibility / Q000097:blood / Q000209:etiology / Q000378:metabolism; D005260:Female; D005632:Fructose / Q000009:adverse effects* / Q000378:metabolism; D005921:Glomerulonephritis / Q000097:blood / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D018149:Glucose Intolerance / Q000097:blood / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008659:Metabolic Diseases / Q000097:blood / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009765:Obesity / Q000097:blood / Q000209:etiology / Q000378:metabolism; D009929:Organ Size; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000097:blood / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000096:biosynthesis
chemical_list: D001786:Blood Glucose; D016212:Transforming Growth Factor beta; D005632:Fructose