Exploring the psychological wellbeing of women with gestational diabetes mellitus (GDM): increased risk of anxiety in women requiring insulin. A Prospective Longitudinal Observational Pilot Study.

Introduction: Gestational diabetes mellitus (GDM) complicates ∼16% of pregnancies in Australia and has significant implications for health of both mother and baby. Antenatal anxiety and depression are also associated with adverse pregnancy outcomes. The interaction between GDM and mental health in pregnancy is poorly understood.

Utility of antenatal clinical factors for prediction of postpartum outcomes in women with gestational diabetes mellitus (GDM).

Background: Gestational diabetes mellitus (GDM) is associated with life-long increased risk of type 2 diabetes: affected women are advised to undergo oral glucose tolerance testing (OGTT) at 6-12 weeks postpartum, then glucose screening every 1-3 years.

Aims: We investigated whether in women with GDM, antenatal clinical factors predicted postpartum abnormal glucose tolerance and compliance with screening.

Materials And Methods: In women with GDM delivering 2007 to mid-2009 in a single hospital, antenatal/obstetric data and glucose tests at 6-12 weeks postpartum and during 5.

Glycosylated haemoglobin for screening and diagnosis of gestational diabetes mellitus.

Objectives: The oral glucose tolerance test (OGTT) is a cumbersome test that is time consuming, labour intensive and often poorly tolerated by pregnant women. To date, glycosylated haemoglobin (HbA1c) is the most accepted measure of chronic glycaemia outside of pregnancy. HbA1c is an uncomplicated test, less time consuming, does not require any specific patient preparation and is considered straightforward compared with the OGTT.

Obesity-Associated Inflammatory Cytokines and Prostaglandin E2 Stimulate Glucose Transporter mRNA Expression and Glucose Uptake in Primary Human Adipose Stromal Cells.

Obesity is associated with chronic low-grade inflammation. This occurs largely as a result of the infiltration of immune cells within the obese adipose, which produce a number of inflammatory factors, including interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNFα), and prostaglandin E(2) (PGE(2)). These factors have previously been shown to affect insulin-mediated glucose uptake in differentiated adipocytes.

Interrelationships of serum androgens, omental adipose tissue metabolism, and nonalcoholic fatty liver disease in obese premenopausal women.

Background: The concept that androgens regulate multiple aspects of adipose tissue metabolism in women is based on studies of women with pathological androgen excess and in vitro studies generally using supraphysiological androgen concentrations. We investigated whether in women with normal-range serum testosterone, relationships exist between serum androgens and expression of proinflammatory (tumor necrosis factor-α, interleukin-6, CD68), anti-inflammatory (adiponectin), and lipid metabolic (lipoprotein lipase, hormone sensitive lipase) genes in omental adipose tissue, and severity of nonalcoholic fatty liver disease (NAFLD).

Methods: We studied obese women undergoing laparoscopic gastric band surgery (premenopausal, regular menses, nondiabetic, serum testosterone <2.

Fasting blood glucose predicts response to extended-release metformin in gestational diabetes mellitus.

Background: Metformin is increasingly accepted as an alternative to insulin therapy in gestational diabetes mellitus (GDM). The Metformin in Gestational Diabetes (MiG) trial reported similar pregnancy outcomes for metformin versus insulin; however, supplemental insulin was required in 46% of women on metformin.

Aims: We aimed to identify predictors of response to metformin monotherapy in women with GDM attending a general hospital antenatal clinic.

Insulin resistance in skeletal muscle and adipose tissue in polycystic ovary syndrome: are the molecular mechanisms distinct from type 2 diabetes?

The association of polycystic ovary syndrome (PCOS) with insulin resistance was recognized almost three decades ago. Despite the pivotal role of insulin resistance in the pathogenesis of PCOS, the precise cellular and molecular mechanisms of impaired insulin action remain elusive. This review has two aims: 1) to review the mechanisms of insulin resistance, specifically impaired insulin-stimulated glucose transport, in skeletal muscle and adipose tissue in PCOS, and 2) to assess whether mechanisms of insulin resistance in PCOS are distinct from those in type 2 diabetes.

Effects of androgens on insulin action in women: is androgen excess a component of female metabolic syndrome?

Hyperinsulinemia as a consequence of insulin resistance causes hyperandrogenemia in women. The objective was to review evidence for the converse situation, i.e.

Effects of spironolactone on glucose transport and interleukin-6 secretion in adipose cells of women.

Adipose tissue inflammation and insulin resistance are central to the pathogenesis of the metabolic syndrome. Spironolactone, an antagonist of mineralocorticoid receptor, glucocorticoid receptor and androgen receptor, and agonist of progesterone receptor, has anti-inflammatory activity. Blockade of the renin-angiotensin-aldosterone system has been shown to improve glucose metabolism.

The adipose cell lineage is not intrinsically insulin resistant in polycystic ovary syndrome.

Selective resistance to the effects of insulin on glucose metabolism in skeletal muscle and adipose tissue is a key feature of polycystic ovary syndrome (PCOS). The pathogenesis of insulin resistance in skeletal muscle in PCOS involves interaction of in vivo environmental factors with intrinsic defects in insulin signaling. We aimed to determine whether (1) intrinsic defects in insulin action/signaling and cytokine secretion were present in adipose cells in PCOS and (2) insulin resistance can be induced in control adipose cells by culture in medium conditioned by insulin-resistant PCOS fibroblasts.

Chronic testosterone treatment induces selective insulin resistance in subcutaneous adipocytes of women.

Adipose tissue plays a central role in determining whole body insulin sensitivity. Several aspects of adipose cell function are regulated by androgens. Given that high androgen levels and insulin resistance are linked in women, we proposed that androgens may influence insulin-mediated glucose metabolism in adipose cells.

Regulation of adenosine 5',monophosphate-activated protein kinase and lipogenesis by androgens contributes to visceral obesity in an estrogen-deficient state.

Menopause is associated with an accumulation of visceral fat. An emerging concept suggests that relatively elevated levels of circulating androgens, compared with estrogens in postmenopausal women, underlie this shift in body fat distribution. In this study we administered dihydrotestosterone (DHT) to ovariectomized mice to examine the effect of relative androgen excess on adipose tissue distribution and function in estrogen-deficient mice.

Enhanced mitogenic signaling in skeletal muscle of women with polycystic ovary syndrome.

Insulin resistance in polycystic ovary syndrome (PCOS) results from a postbinding defect in signaling. Insulin receptor and insulin receptor substrate (IRS)-1 serine hyperphosphorylation by an unidentified kinase(s) contributes to this defect. We investigated whether insulin resistance is selective, affecting metabolic but not mitogenic pathways, in skeletal muscle as it is in cultured skin fibroblasts in PCOS.

Insulin resistance in the skeletal muscle of women with PCOS involves intrinsic and acquired defects in insulin signaling.

Insulin resistance in polycystic ovary syndrome (PCOS) is due to a postbinding defect in signaling that persists in cultured skin fibroblasts and is associated with constitutive serine phosphorylation of the insulin receptor (IR). Cultured skeletal muscle from obese women with PCOS and age- and body mass index-matched control women (n = 10/group) was studied to determine whether signaling defects observed in this tissue in vivo were intrinsic or acquired. Basal and insulin-stimulated glucose transport and GLUT1 abundance were significantly increased in cultured myotubes from women with PCOS.

The effect of obesity on the ratio of type 3 17beta-hydroxysteroid dehydrogenase mRNA to cytochrome P450 aromatase mRNA in subcutaneous abdominal and intra-abdominal adipose tissue of women.

Objectives: To investigate (1) whether type 3 17beta-hydroxysteroid dehydrogenase (17beta-HSD), the enzyme which catalyzes the conversion of androstenedione to testosterone in the testis, is co-expressed with P450aromatase in the preadipocytes of women, and (2) whether the relative expression of type 3 17beta-HSD and aromatase varies in subcutaneous abdominal vs intra-abdominal adipose tissue of women.

Subjects: Subcutaneous abdominal and intra-abdominal adipose tissue was obtained from women undergoing elective abdominal surgery (age 22-78 y, body mass index (BMI) 22.4-52.

Insulin resistance in polycystic ovary syndrome: progress and paradoxes.

Over the past 20 years, it has been clearly documented that 1) polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resistance and 2) insulin resistance plays an important role in the pathogenesis of the reproductive abnormalities of the disorder. Women with PCOS are at significantly increased risk of developing type 2 diabetes mellitus (DM). Studies in isolated adipocytes and in cultured skin fibroblasts from PCOS women have demonstrated intrinsic postbinding defects in insulin-mediated glucose metabolism.

Insulin/IGF-1 and TNF-alpha stimulate phosphorylation of IRS-1 at inhibitory Ser307 via distinct pathways.

Serine/threonine phosphorylation of IRS-1 might inhibit insulin signaling, but the relevant phosphorylation sites are difficult to identify in cultured cells and to validate in isolated tissues. Recently, we discovered that recombinant NH2-terminal Jun kinase phosphorylates IRS-1 at Ser307, which inhibits insulin-stimulated tyrosine phosphorylation of IRS-1. To monitor phosphorylation of Ser307 in various cell and tissue backgrounds, we prepared a phosphospecific polyclonal antibody designated alphapSer307.

Expression of types 1, 2, and 3 17 beta-hydroxysteroid dehydrogenase in subcutaneous abdominal and intra-abdominal adipose tissue of women.

Human adipose tissue is known to have 17 beta-oxidoreductase activity, interconverting estrone (E1) and estradiol (E2), as well as androstenedione (A) and testosterone (T). We examined both the subcutaneous abdominal and intra-abdominal (visceral) adipose tissue of women for expression of types 1, 2, and 3 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) using ribonuclease (RNase) protection assay and RT-PCR/Southern blotting. Type 1 17 beta-HSD, which encodes the enzyme responsible for the conversion of E1 to E2 in the placenta and ovary, was expressed in the subcutaneous abdominal and intra-abdominal adipose tissue of women, but the messenger RNA transcripts were predominantly incompletely spliced and therefore unlikely to encode an active protein.

Regulation of the insulin-like growth factors and their binding proteins by glucocorticoid and growth hormone in nonislet cell tumor hypoglycemia.

Hypoglycemia in patients with nonislet cell tumors is often secondary to overexpression of tumor insulin-like growth factor (IGF) II. In these patients the formation of serum complexes between IGFs, IGF binding protein-3 (IGFBP-3), and the acid-labile subunit (ALS) is impaired. An 87-yr-old woman with nonislet cell tumor hypoglycemia resulting from a localized fibrous tumor of the pleura was treated for 97 days with graded doses of prednisolone (30, 10, and 5 mg/day) followed by GH (1, 4, 8, 4, and 2 U/day).

Serological studies of Australian and Papua New Guinean cattle and Australian sheep for the presence of antibodies against bluetongue group viruses.

Following isolation of a virus (CSIRO19) from insects in Australia and its identification as bluetongue virus serotype 20 (BTV20), a nationwide survey of antibodies in cattle and sheep sera was undertaken. Initial studies using the serum neutralization (SN) test showed that the distribution of BTV20 antibodies in cattle was confined to the northern part of Australia. Group-reactive antibody tests (agar gel diffusion precipitin, AGDP, and complement-fixation, CF) showed group-reactive cattle sera south of the BTV20 zone (northern Australia), and southwards from Queensland to New South Wales.