E. Gregoraszczuk1, M. Slupecka2, J. Wolinski2, A. Hejmej3, B. Bilinska3, E. Fiedor1, N. Piwnicka1, A. Rak1 Maternal High-fat Diet during Pregnancy and Lactation Had Gender Difference Effect on Adiponectin in Rat Offspring

One emerging issue of great concern in reproductive health and obesity is the intergenerational implications of obesity, as well as consumption of fat diet during pregnancy. There is evidence from epidemiological and animal studies suggesting that the intrauterine environment in obese women can impact on both female and male offspring. It is becoming apparent, therefore, that a woman's nutritional and metabolic status during pregnancy can programme her daughter or son, and in the case of the daughter when she reaches childbearing age, she can in turn impose an effect on the next generation (1). Previous research has shown that too much or too little nutrition during fetal life resulted in profound and permanent changes in their development including alterations in the structure of the liver, brain and pancreas that increase their susceptibility to developing various diseases later in life, including obesity, diabetes and cardiovascular disease. Krasnow et al. (2), using a mouse model to examine how consumption of a HF diet during pregnancy affects body composition in the newborn, showed that on the day of birth, babies born to females who had consumed HF food had more body fat, less lean mass, and smaller livers than the newborns of females that consumed low-fat food. Adipose tissue is an important source of hormones that influence both metabolism and reproduction (3). It is well known that both obesity and excessive leanness are associated with reproductive dysfunction. Recent investigations have yielded new information on the endocrine role of white adipose tissue (WAT) via the expression of protein messengers known as adipokines (4). Although adipose tissue secretes a variety of factors, only leptin and adiponectin (and possibly resistin, adipsin, and visfatin) are primarily produced by adipocytes and can therefore be properly classified as adipokines. Wronska et al., (5) observed that metabolic effects of short-term calorie restriction with subsequent refeeding in WAT depots of young and old Wistar rats was associated with increase in serum leptin concentration. Adiponectin secretion is related to the abundance of the adipose tissue and is regulated by autocrine and endocrine factors, predominately by gonadal steroids (6, 7). The production and secretion of adiponectin is inversely correlated to the severity of obesity. Women display higher circulating adiponectin levels than men, and weight loss in both is characterized by increases in adiponectin levels in the plasma (8). Adiponectin was first described in 1995 as adipocyte complement-related protein of 30 kDa (Acrp30) (9). Adiponectin mediates its action in the periphery principally through two receptors, AdipoR1 and AdipoR2 (9). The effects of adipokines on the process of ovulation and ovarian steroidogenesis have not been extensively studied, however JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY 2016, 67, 4, 543-553