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ARS Home » Southeast Area » Little Rock, Arkansas » Microbiome and Metabolism Research Unit » Research » Publications at this Location » Publication #347395

Title: Maternal high-fat diet modulates brown adipose tissue response to B-adrenergic agonist

item WANKHADE, UMESH - Arkansas Children'S Nutrition Research Center (ACNC)
item KANG, PING - Arkansas Children'S Nutrition Research Center (ACNC)
item ZHONG, YING - Arkansas Children'S Nutrition Research Center (ACNC)
item THAKALI, KESHARI - Arkansas Children'S Nutrition Research Center (ACNC)
item SHANKAR, KARTIK - Arkansas Children'S Nutrition Research Center (ACNC)

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 9/1/2017
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Maternal obesity increases offspring risk for several metabolic diseases. We previously showed that offspring of obese dams are predisposed to obesity, liver and adipose tissue anomalies. However, the effect of maternal obesity on developmental programing brown adipose tissue (BAT) is poorly understood. By using a mouse model of HFD-induced obesity, we investigated changes in BAT following B3-adrenergic receptor (B3AR) agonist, CL-316243 treatment. Female C57BL6/J dams were fed either control (17% fat) or HFD (45% fat) and bred with lean male mice. Following weaning, offspring from both diet groups remained on control diets (CC, HC respectively). At 20 weeks of age, offspring were treated with vehicle or B3-adrenergic receptor agonist CL-316243 (CL, 1 mg/kg i.p. for one week, n=4-5). H&E staining revealed larger adipocytes and more lipid deposition in BAT of offspring of HFD dams. Global RNA transcriptomic analysis revealed distinct effect of maternal HFD feeding. Principal component analysis revealed clustering of samples based on the maternal diet. Maternal HFD altered expression of 89 genes (+/2-fold change, adj p<0.05). Enrichment of gene ontology biological processes revealed genes related to cellular metabolic process, response to stress, chemical, temperature stimulus and heat. Following CL-316243 treatment HC offspring showed impaired physiological responses. Classical BAT specific proteins such as Ucp1, Dio2 and Cidea were downregulated in BAT of HC offspring upon CL-316243 challenge. In addition, protein kinases such as AMPK as well as ERK1/2 were also down regulated in HC groups treated with CL-316243. In conclusion, our results indicate that maternal obesity programs adipose tissue response to the B3AR stimulation which may influence pathways regulating energy expenditure, metabolism and overall risk of obesity.