Effects of maternal exercise on infant mesenchymal stem cell mitochondrial function, insulin action, and body composition in infancy.

Maternal exercise (ME) has been established as a useful non-pharmacological intervention to improve infant metabolic health; however, mechanistic insight behind these adaptations remains mostly confined to animal models. Infant mesenchymal stem cells (MSCs) give rise to infant tissues (e.g., skeletal muscle), and remain involved in mature tissue maintenance. Importantly, these cells maintain metabolic characteristics of an offspring donor and provide a model for the investigation of mechanisms behind infant metabolic health improvements. We used undifferentiated MSC to investigate if ME affects infant MSC mitochondrial function and insulin action, and if these adaptations are associated with lower infant adiposity. We found that infants from exercising mothers have improvements in MSC insulin signaling related to higher MSC respiration and fat oxidation, and expression and activation of energy-sensing and redox-sensitive proteins. Further, we found that infants exposed to exercise in utero were leaner at 1 month of age, with a significant inverse correlation between infant MSC respiration and infant adiposity at 6 months of age. These data suggest that infants from exercising mothers are relatively leaner, and this is associated with higher infant MSC mitochondrial respiration, fat use, and insulin action.

Differences in substrate metabolism between African American and Caucasian infants: evidence from mesenchymal stem cells.

Type 2 diabetes is more prevalent in African American (AA) than Caucasian (C) adults. Furthermore, differential substrate utilization has been observed between AA and C adults, but data regarding metabolic differences between races at birth remains scarce. The purpose of the present study was to determine if there are racial differences in substrate metabolism evident at birth using a mesenchymal stem cells (MSCs) collected from offspring umbilical cords. Using radio-labeled tracers, MSCs from offspring of AA and C mothers were tested for glucose and fatty acid metabolism in the undifferentiated state and while undergoing myogenesis in vitro. Undifferentiated MSCs from AA exhibited greater partitioning of glucose toward nonoxidized glucose metabolites. In the myogenic state, AA displayed higher glucose oxidation, but similar fatty acid oxidation rates. In the presence of both glucose and palmitate, but not palmitate only, AA exhibit a higher rate of incomplete fatty acid oxidation evident by a greater production of acid-soluble metabolites. Myogenic differentiation of MSCs elicits an increase in glucose oxidation in AA, but not in C. Together, these data suggest that metabolic differences between AA and C races exist at birth.NEW & NOTEWORTHY African Americans, when compared with Caucasians, display greater insulin resistance in skeletal muscle. Differences in substrate utilization have been proposed as a factor for this health disparity; however, it remains unknown how early these differences manifest. Using infant umbilical cord-derived mesenchymal stem cells, we tested for in vitro glucose and fatty acid oxidation differences. Myogenically differentiated MSCs from African American offspring display higher rates of glucose oxidation and incomplete fatty acid oxidation.

Postpartum prolapsed leiomyoma with uterine inversion managed by vaginal hysterectomy.

Background. Uterine inversion is a rare, but life threatening, obstetrical emergency which occurs when the uterine fundus collapses into the endometrial cavity. Various conservative and surgical therapies have been outlined in the literature for the management of uterine inversions. Case. We present a case of a chronic, recurrent uterine inversion, which was diagnosed following spontaneous vaginal delivery and recurred seven weeks later. The uterine inversion was likely due to a leiomyoma. This late-presenting, chronic, recurring uterine inversion was treated with a vaginal hysterectomy. Conclusion. Uterine inversions can occur in both acute and chronic phases. Persistent vaginal bleeding with the appearance of a prolapsing fibroid should prompt further investigation for uterine inversion and may require surgical therapy. A vaginal hysterectomy may be an appropriate management option in select populations and may be considered in women who do not desire to maintain reproductive function.

Surgical management of massive labial edema in a gravid preeclamptic diabetic.

Background. Massive labial edema is a rare complication during pregnancy that can jeopardize vaginal delivery, as well as leading to maternal and fetal morbidity. It can be related to systemic pathologies, but has been commonly associated with preeclampsia and diabetes. This increased and sometimes longstanding pressure may result in a "labial compartment syndrome" leading to microvascular damage and tissue necrosis if not resolved in a timely fashion. Case. Massive labial edema was treated first conservatively and then surgically in a gravid diabetic patient with severe preeclampsia. Immediately after Cesarean section, the labial compartment syndrome was relieved surgically and resolved rapidly. Conclusion. When conservative attempts at management of labial edema fail, or rapid resolution is critical to maternal and fetal outcome, surgical alternatives should be considered.

Uterine hyperstimulation by intravenous access in a mammary vein: a case report and literature review.

Breast stimulation can produce contractions in a contraction stress test and has been considered for the augmentation of labor and prevention of postpartum hemorrhage. We present a case of intravenous access of a mammary vein in an obstetric patient that led to uterine hyperstimulation. Potential dangers of mammary vein intravenous access are discussed.

Gestational diabetes is associated with depressed adiponectin levels.

OBJECTIVE: Adiponectin is a 29-kd adipocyte-secreted protein that has been linked to insulin resistance in obesity and diabetes. The aim of the present study was to evaluate adiponectin levels in the insulin-resistant state of diabetes in gestation. METHODS: Term, gravid subjects with diabetes (n = 31; age, 30.0 +/- 0.9 years; weight, 98.8 +/- 4.6 kg) and healthy, term, gravid subjects (n = 27; age, 26.1 +/- 1.1 years; weight, 91.2 +/- 3.78 kg) were examined. The diabetes group consisted of 11 class A1, 11 class A2, and nine class B subjects. Plasma insulin, glucose, adiponectin, and leptin were measured on samples obtained immediately before Cesarean or vaginal delivery. Data were presented as means +/- SE, and significance is set at P < or = .05. RESULTS: We observed decreased adiponectin levels in class A2 (4.93 +/- 0.58 microg/mL; P = .013) and class B diabetics (3.33 +/- 0.56 microg/mL; P = .001) as compared to controls (8.17 +/- 0.82 microg/mL), while a nonsignificant decrease was also observed in class A1 (6.58 +/- 1.13 microg/mL; P = .213). When grouping all gravid subjects, we observed that non-Caucasian subjects (n = 42) (5.51 +/- 0.51 microg/mL; P = .003) had lower adiponectin levels than Caucasian subjects (n = 16) (8.88 +/- 1.11 microg/mL). Within the non-Caucasian group, we found significantly lower adiponectin levels in diabetic gravid subjects (class A2: 4.24 +/- 0.75 microg/mL; P = .044; and class B: 3.33 +/- 0.56 microg/mL; P = .005) compared with nondiabetic gravid subjects (7.05 +/- 0.80 microg/mL). CONCLUSION: Class A2 and B gestational diabetes are associated with suppressed levels of adiponectin, similar to that found in other insulin-resistant states (type II diabetes and obesity).