title: Oestrogen alters adipocyte biology and protects female mice from adipocyte inflammation and insulin resistance.
abstract: OBJECTIVE
  Obesity is associated with insulin resistance, liver steatosis and low-grade inflammation. The role of oestrogen in sex differences in the above co-morbidities is not fully understood. Our aim was to assess the role oestrogen has in modulating adipocyte size, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis.
  
  
  METHODS
  To determine the role oestrogen has in the above co-morbidities related to obesity, we randomized C57BL/6J mice into four groups (15 mice per group): (i) male, (ii) non-ovariectomized female (novx), (iii) ovariectomized female (ovx) and (iv) ovariectomized female mice supplemented with 17β estradiol (ovx-E). Mice received either a low-fat (LF) or a high-fat (HF) diet for 10 weeks. Outcomes measured were bodyweight, body fat, adipocyte diameter, adipose tissue lipolysis markers, adipose tissue oxidative stress, inflammation, insulin resistance and liver steatosis.
  
  
  RESULTS
  Male and ovx-female mice consuming the HF diet had a higher propensity of gaining weight, specifically in the form of body fat. Oestrogen protected female mice from adipocyte hypertrophy and from developing adipose tissue oxidative stress and inflammation. Moreover, novx-female and ovx-female+E mice had higher phosphorylated levels of protein kinase A and hormone sensitive lipase, markers associated with lipolysis. Additionally, male and ovx female mice had a higher propensity of developing liver steatosis and insulin resistance. In contrast, oestrogen protected female mice from developing liver steatosis and from becoming insulin resistant.
  
  
  CONCLUSIONS
  We show that oestrogen protects female mice from adipocyte hypertrophy and adipose tissue oxidative stress and inflammation. Furthermore, oestrogen prevented female mice from developing liver steatosis and from becoming insulin resistant.
authors.affiliation: Department of Nutritional Sciences, University of Texas at Austin, Austin, TX 78712, USA.
authors.forename: R E
authors.initials: RE
authors.lastname: Stubbins
authors.forename: K
authors.initials: K
authors.lastname: Najjar
authors.forename: V B
authors.initials: VB
authors.lastname: Holcomb
authors.forename: J
authors.initials: J
authors.lastname: Hong
authors.forename: N P
authors.initials: NP
authors.lastname: Núñez
mesh_terms: D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000187:drug effects* / Q000378:metabolism; D001835:Body Weight; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology*; D005234:Fatty Liver / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control*; D005260:Female; D006984:Hypertrophy / Q000517:prevention & control; D007249:Inflammation / Q000378:metabolism; D007333:Insulin Resistance; D008066:Lipolysis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000188:drug therapy / Q000378:metabolism*; D010052:Ovariectomy; D011897:Random Allocation; D014280:Triglycerides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D004967:Estrogens; D014280:Triglycerides