16, 18- 21īrown adipose tissue (BAT) has recently emerged as a possible therapeutic target to counteract obesity and insulin resistance in humans. 9- 18 The mechanisms by which offspring develop cardiovascular disease have been linked to epigenetic changes, endothelial dysfunction, inflammation, oxidative stress, lipogenesis, nonalcoholic fatty liver disease, adipocyte hypertrophy, pancreatic abnormalities, and alterations in hypothalamic satiety signaling. Multiple animal studies have shown that offspring born of pregnancies complicated by obesity are at increased risk of obesity, increased blood pressure, and other features of MetS. While epidemiological studies provide important insight into the origins of obesity in humans, animal models remain essential for confirming the epidemiological associations, studying the mechanisms involved, and developing novel therapies. Thus, maternal obesity is a significant factor contributing to increased risk of obesity in offspring. 12 Adults born to obese mothers were more insulin resistant than those born to nonobese mothers. 11 Maternal BMI was found to be one of the strongest predictors of excessive weight and obesity in sons at 18 years. 10 MetS is more common in adolescents who were large-for-gestational-age at birth or who were born to obese mothers. 9 After controlling for confounders, the relative risk of childhood obesity associated with maternal obesity in the first trimester of pregnancy has been found to increase 2-fold at 2-3 years of age and 2.3-fold at 4 years.

6- 8Įpidemiological studies have shown that children born of pregnancies complicated by obesity are at increased risk of obesity and other features of MetS. 5 Furthermore, the prevalence of obesity in pregnancy in the US ranges between 18.5% and 38.3%, and these rates continue to rise. 4 In the US, almost one-third of women of reproductive age (20-39 years) are obese. 3 In 2003, the prevalence of overweight and obese women reached 61.6%. The proportion of women who are obese has doubled since the 1960s.

Traditionally, research into the causes of obesity has focused on lifestyle factors in childhood and adulthood, but recently the role of pregnancy in fueling the obesity epidemic has begun to be recognized. Moreover, an estimated 15% of US adults have 1 or more of these conditions without a diagnosis. Of the 3 most common chronic conditions associated with MetS-namely, hypertension, hypercholesterolemia, and diabetes-45% of adults are reported to have at least 1, 13% to have 2, and 3% to have all 3 conditions. 1 Obesity is one of the key risk factors in the development of MetS. Prenatal exposure to maternal obesity leads to significant increases in UCP1 levels and function in BAT in offspring with little impact on UCP1 levels and function in SAT and VAT.Īccording to the National Health and Nutrition Examination Survey (NHANES, 2003–2006), 34% of adults in the US meet the criteria for metabolic syndrome (MetS), a cluster of major cardiovascular risk factors related to obesity and insulin resistance. There were no differences in total respiration in SAT and VAT. In VAT, UCP1 protein levels and UCPl-dependent respiration were significantly lower only in HF females ( P =. 03), and the UCPl-dependent thermogenesis was significantly lower from HF males ( P =. In SAT, the UCPl protein were significantly lower in HF females ( P =. UCP1 protein levels, total mitochondrial respiration, and UCPl-dependent respiration were significantly higher in BAT from HF males ( P =. UCP1 mRNA levels were not different between the HF and SF offspring. A Student t test and Mann-Whitney test were used (significance: P <.

Total and UCPl-dependent mitochondrial respiration were determined by high-resolution respirometry. UCP1 mRNA and protein levels were quantified using q RT-PCR and Western blot analysis, respectively, in brown (BAT), subcutaneous (SAT), and visceral (VAT) adipose tissues at 6 months of age. After weaning, all pups were placed on SF. Female CD-1 mice were fed a high-fat (HF) or standard fat (SF) diet for 3 months before breeding. We investigated if levels of Uncoupling Protein 1 (UCP1) and UCP1- mediated thermogenesis are altered in offspring exposed to prenatal obesity.

With brown adipose tissue (BAT) becoming a possible therapeutic target to counteract obesity, the prenatal environment could represent a critical window to modify BAT function and browning of white AT.

Staring at the sun offspring