Objective We determined the potential programming effects of maternal obesity and high fat (HF) diet during pregnancy and/or lactation on offspring metabolic syndrome. Study Design A rat model of maternal obesity was created using a HF diet prior to and throughout pregnancy and lactation. At birth, pups were cross fostered thereby generating four paradigms of maternal diets during pregnancy/lactation: (1) control (Con) diet during pregnancy and lactation - Con/Con, (2), HF during pregnancy and lactation - HF/HF, (3) HF during pregnancy alone - HF/Con, and (4) HF during lactation alone - Con/HF. Results Maternal phenotype during pregnancy and the end of lactation evidenced markedly elevated body fat and plasma corticosterone levels in HF dams. In the offspring, maternal HF diet during pregnancy alone programmed increased offspring adiposity, though with normal body weight, whereas maternal HF diet during lactation increased both body weight and adiposity. Metabolic disturbances, particularly that of hyperglycemia, were apparent in all groups exposed to maternal HF diet (during pregnancy and/or lactation), though differences were apparent in the manifestation of insulin resistant versus insulin deficient phenotypes. Elevated systolic blood pressure was manifest in all groups implying that exposure to an obese/HF environment is disadvantageous for offspring health, regardless of pregnancy or lactation periods. Nonetheless, the underlying mechanism may differ as offspring that experienced in utero HF exposure had increased corticosterone levels. Conclusion Maternal obesity/HF diet markedly impact offspring body composition and the risk of metabolic syndrome dependent upon period of exposure during pregnancy and/or lactation.

The metabolic syndrome epidemic, including a marked increase in the prevalence of obesity and gestational diabetes mellitus (GDM) among pregnant women, represents a significant public health problem. There is increasing recognition that the risk of adult obesity is clearly influenced by prenatal and infant environmental exposures, particularly nutrition. This tenet is the fundamental basis of developmental programming. Low birth weight, together with infant catch-up growth, is associated with a significant risk of adult obesity. Exposure to maternal obesity, with or without GDM, or having a high birth weight also represents an increased risk for childhood and adult obesity. Animal models have replicated human epidemiologic findings and elucidated potential programming mechanisms that include altered organ development, cellular signaling responses, and epigenetic modifications. Prenatal care has made great strides in optimizing maternal, fetal, and neonatal health, and now has the opportunity to begin interventions which prevent or reduce childhood/adult obesity. Guidelines that integrate optimal pregnancy nutrition and weight gain, management of GDM, and newborn feeding strategies with long-term consequences on adult obesity, remain to be elucidated.

Fetal intrauterine growth restriction has been associated with adult disease in both human epidemiologic studies and in animal models. In some cases, intrauterine deprivation programs the fetus to develop increased appetite and obesity, hypertension and diabetes as an adult. Although the mechanisms responsible for fetal programming remain poorly understood, both anatomic and functional (cell signaling) changes have been described in affected individuals. In some animal models, aspects of fetal programming can be reversed postnatally, however at the present time the best strategy for avoiding the adult consequences of fetal growth restriction is prevention.Fetal intrauterine growth restriction (IUGR) occurs in humans as a consequence of poor maternal nutrition, placental insufficiency and diminished fetal oxygenation, or exposure to teratogens, among other causes. In animals, and in some cases in humans, IUGR from these causes has been associated with the development of adult diseases; this phenomenon is called "fetal programming". The association of maladaptive programming with adult disease has been termed the "Barker hypothesis". In general, the Barker hypothesis 1 contends that the malnourished fetus is programmed to exhibit a "thrifty phenotype" with increased food intake and fat deposition and possibly decreased energy output. Faced with ample available calories, such individuals develop obesity and other manifestations of the metabolic syndrome as adults due to alterations in homeostatic regulatory mechanisms. 2-4The issue of fetal programming is not merely of intellectual interest. Currently, 65% of adults in the United States are overweight and almost one in three are obese (BMI>30 kg/m 2 ), representing a modern health crisis. 5 Obesity and its related diseases are the leading cause of death in Western society, with associated risks of hypertension, coronary heart disease, stroke, diabetes, and breast, prostate and colon cancer. Evidence indicates a striking 25 to 63% of adult diabetes, hypertension and coronary heart disease can be attributed to the effects of low birthweight with accelerated newborn-to-adolescent weight gain. 2 therefore gestational programming of low birth weight/ IUGR has contributed importantly to the population shift towards obesity. In Western societies, the incidence of low birth weight infants has increased since the mid-twentieth century. Low birth weight infants are now being born to women with chronic diseases who would previously have had limited survival and reproductive capacity, while assisted reproductive technologies and increasing numbers of multiple gestations have resulted in both preterm and low birth weight offspring. When combined with improved

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The incidence of shoulder dystocia, as defined by the use of ancillary obstetric maneuvers, is higher than that reported previously, and the reporting of shoulder dystocia appears to be unreliable. The interval from head-to-body delivery is delayed significantly in patients with shoulder dystocia, despite the lack of recognition of shoulder dystocia. We propose defining shoulder dystocia as a prolonged head-to-body delivery time (eg, more than 60 seconds) or the need for ancillary obstetric maneuvers.

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Neonatal clavicle fracture is associated with infant birth weight greater than 4 kg, but not with the occurrence of objectively defined shoulder dystocia. However, infants with clavicle fracture may be at increased risk for additional complications.