CGM use may be beneficial in insulin-treated GDM because it improves HbA compared with usual antenatal care without increasing severe hypoglycaemia. (Clinical Trials Registry No.: NCT02204657).

Generally, obese and overweight individuals display higher free fatty acid levels, which stimulate insulin resistance. The combination of overweight or obesity with insulin resistance can trigger Type 2 diabetes mellitus (T2DM) and are primary contributing factors to the development of uncontrolled T2DM. Genetic polymorphisms also play an important role as they can impact a population's susceptibility to becoming overweight or obese and developing related chronic complications, such as uncontrolled T2DM. This review specifically examines the genetic polymorphisms associated with overweight and obesity in patients with uncontrolled T2DM. Particularly, gene polymorphisms in ADIPOQ (rs1501299 and rs17300539), LepR (rs1137101 and rs1045895), IRS2 (rs1805092), GRB14 (rs10195252 and rs3923113) and PPARG (rs1801282) have been associated with overweight and obesity in uncontrolled T2DM.

Despite low awareness and detection rates, HP dysfunction post-NPC irradiation is common. Use of CCRT may augment time related pituitary damage. As these endocrinopathies result in significant morbidity and mortality we recommend periodic assessment of pituitary function amongst NPC survivors.

Objective To determine the association between maternal lipaemia and neonatal anthropometrics in Malaysian mother-offspring pairs. Design Prospective observational cohort study.Setting Single tertiary multidisciplinary antenatal clinic in Malaysia.Population A total of 507 mothers: 145 with gestational diabetes mellitus (GDM); 94 who were obese with normal glucose tolerance (NGT) (pre-gravid body mass index, BMI ≥ 27.5 kg/m 2 ), and 268 who were not obese with NGT.Methods Maternal demographic, anthropometric, and clinical data were collected during an interview/examination using a structured questionnaire. Blood was drawn for insulin, C-peptide, triglyceride (Tg), and non-esterified fatty acid (NEFA) during the 75-g 2-hour oral glucose tolerance test (OGTT) screening, and again at 36 weeks of gestation. At birth, neonatal anthropometrics were assessed and data such as gestational weight gain (GWG) were extracted from the records.Main outcome measures Macrosomia, large-for-gestational-age (LGA) status, cohort-specific birthweight (BW), neonatal fat mass (NFM), and sum of skinfold thickness (SSFT) > 90th centile.Results Fasting Tg > 95th centile (3.6 mmol/L) at screening for OGTT was independently associated with LGA (adjusted odds ratio, aOR 10.82, 95% CI 1.26-93.37) after adjustment for maternal glucose, pre-gravid BMI, and insulin sensitivity. Fasting glucose was independently associated with a birthweight ratio (BWR) of >90th centile (aOR 2.06, 95% CI 1.17-3.64), but not with LGA status, in this well-treated GDM cohort with predelivery HbA1c of 5.27%. In all, 45% of mothers had a pre-gravid BMI of <23 kg/m 2 and 61% had a pre-gravid BMI of ≤ 25 kg/m 2 , yet a GWG of >10 kg was associated with a 4.25-fold risk (95% CI 1.71-10.53) of BWR > 90th centile.Conclusion Maternal lipaemia and GWG at a low threshold (>10 kg) adversely impact neonatal adiposity in Asian offspring, independent of glucose, insulin resistance and pre-gravid BMI. These may therefore be important modifiable metabolic targets in pregnancy.

Aims/IntroductionStudies on the relative contributions of fasting and postprandial hyperglycemia (FH and PPH) to glycated hemoglobin (HbA1c) in patients with type 2 diabetes have yielded inconsistent results. We aimed to assess the relationship by using continuous glucose monitoring in a multi‐ethnic cohort.Materials and MethodsA total of 100 adults with type 2 diabetes were assessed with 6‐day continuous glucose monitoring and HbA1c. Area under the curve (AUC) ≥5.6 mmol/L was defined as AUCTOTAL. AUC equal to or greater than each preprandial glucose for 4‐h duration was defined as AUCPPH. The total PPH (AUCTPPH) was the sum of the various AUCPPH . The postprandial contribution to overall hyperglycemia was calculated as (AUCTPPH / AUCTOTAL) × 100%.ResultsThe present study comprised of Malay, Indian, and Chinese type 2 diabetes patients at 34, 34 and 28% respectively. Overall, the mean PPH significantly decreased as HbA1c advanced (mixed model repeated measures adjusted, beta‐estimate = −3.0, P = 0.009). Age (P = 0.010) and hypoglycemia (P = 0.006) predicted the contribution difference. In oral antidiabetic drug‐treated patients (n = 58), FH contribution increased from 54% (HbA1c 6–6.9%) to 67% (HbA1c ≥10%). FH predominance was significant in poorly‐controlled groups (P = 0.028 at HbA1c 9–9.9%; P = 0.015 at HbA1c ≥10%). Among insulin users (n = 42), FH predominated when HbA1c was ≥10% before adjustment for hypoglycemia (P = 0.047), whereas PPH was numerically greater when HbA1c was <8%.Conclusions FH and PPH contributions were equal in well‐controlled Malaysian type 2 diabetes patients in real‐world practice. FH predominated when HbA1c was ≥9 and ≥10% in oral antidiabetic drug‐ and insulin‐treated patients, respectively. A unique observation was the greater PPH contribution when HbA1c was <8% despite the use of basal and mealtime insulin in this multi‐ethnic cohort, which required further validation.