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Barnes, R. A., et al. (2019). "Excessive Weight Gain Before and During Gestational Diabetes Mellitus Management: What Is the Impact?" Diabetes Care 43(1): 74-81 FULL TEXT @ SWSLHD https://doi.org/10.2337/dc19-0800
Conventional gestational diabetes mellitus (GDM) management focuses on managing blood glucose in order to prevent adverse outcomes. We hypothesized that excessive weight gain at first presentation with GDM (excessive gestational weight gain [EGWG]) and continued EGWG (cEGWG) after commencing GDM management would increase the risk of adverse outcomes, despite treatment to optimize glycemia. Data collected prospectively from pregnant women with GDM at a single institution were analyzed. GDM was diagnosed on the basis of Australasian Diabetes in Pregnancy Society 1998 guidelines (1992–2015). EGWG means having exceeded the upper limit of the Institute of Medicine–recommended target ranges for the entire pregnancy, by GDM presentation. The relationship between EGWG and antenatal 75-g oral glucose tolerance test (oGTT) values and adverse outcomes was evaluated. Relationships were examined between cEGWG, insulin requirements, and large-for-gestational-age (LGA) infants.Of 3,281 pregnant women, 776 (23.6%) had EGWG. Women with EGWG had higher mean fasting plasma glucose (FPG) on oGTT (5.2 mmol/L [95% CI 5.1–5.3] vs. 5.0 mmol/L [95% CI 4.9–5.0]; P < 0.01), after adjusting for confounders, and more often received insulin therapy (47.0% vs. 33.6%; P < 0.0001), with an adjusted odds ratio (aOR) of 1.4 (95% CI 1.1–1.7; P < 0.01). aORs for each 2-kg increment of cEGWG were a 1.3-fold higher use of insulin therapy (95% CI 1.1–1.5; P < 0.001), an 8-unit increase in final daily insulin dose (95% CI 5.4–11.0; P < 0.0001), and a 1.4-fold increase in the rate of delivery of LGA infants (95% CI 1.2–1.7; P < 0.0001).The absence of EGWG and restricting cEGWG in GDM have a mitigating effect on oGTT-based FPG, the risk of having an LGA infant, and insulin requirements.
Loos, R. J. F. and G. S. H. Yeo (2022). "The genetics of obesity: from discovery to biology." Nature Reviews Genetics 23(2): 120-133 https://doi.org/10.1038/s41576-021-00414-z
The prevalence of obesity has tripled over the past four decades, imposing an enormous burden on people’s health. Polygenic (or common) obesity and rare, severe, early-onset monogenic obesity are often polarized as distinct diseases. However, gene discovery studies for both forms of obesity show that they have shared genetic and biological underpinnings, pointing to a key role for the brain in the control of body weight. Genome-wide association studies (GWAS) with increasing sample sizes and advances in sequencing technology are the main drivers behind a recent flurry of new discoveries. However, it is the post-GWAS, cross-disciplinary collaborations, which combine new omics technologies and analytical approaches, that have started to facilitate translation of genetic loci into meaningful biology and new avenues for treatment.
Monnier, L., et al. (2021). "The obesity treatment dilemma: Why dieting is both the answer and the problem? A mechanistic overview." Diabetes & Metabolism 47(3): 101192 https://www.sciencedirect.com/science/article/pii/S1262363620301270
Restricted-calorie diets are the most worldwide used treatments for obesity. Although such strategies are based on the first law of thermodynamics, the real life clinical practice demonstrates that the observed weight losses are divergent from those theoretically predicted. Loosely adherence to recommendations is one of the main causes for the limited efficacy of dieting, but many additional factors can be involved in the hurdles to weight loss. According to the second law of thermodynamics any restriction in dietary energy intake results in energy sparing with a diminution in the basal metabolic rate and a concomitant loss in the lean body mass. This “thrifty” energetic adaptation is associated with a progressive reduction in the difference between levels of energy intake and expenditure, thus resulting in a drastic fall in weight loss rates on the medium and long-term regardless of the dietary carbohydrate/fat ratio. This loss of efficacy is aggravated by the misadaptation of the production and action of anti-obesity hormones such as leptin. During the latest past decades the discovery of changes in the gut microbiota of obese people referred to as “obese dysbiosis” has raised the question as to whether these alterations can participate to diet-resistance. Combined with the behavioral and psychological barriers to low-calorie diets, there is a broad physiologic spectrum of evidence indicating that weight loss is a hard challenge. Consequently, the answer would be primarily to prevent the development of obesity and at worst to avoid its ominous progression from metabolically healthy to unhealthy stages.
Neto, A. S., et al. (2022). "Clinical outcomes of Indigenous Australians and New Zealand Maori with metabolic acidosis and acidaemia." Critical Care and Resuscitation 24(1): 14-19 Full article at URL https://search.informit.org/doi/10.3316/informit.331866183516118
Objective: To assess the incidence and impact of metabolic acidosis in Indigenous and non-Indigenous patients. Design: Retrospective study. Setting: Adult intensive care units (ICUs) from Australia and New Zealand. Participants: Patients aged 16 years or older admitted to an Australian or New Zealand ICU in one of 195 contributing ICUs between January 2019 and December 2020 who had metabolic acidosis, defined as pH < 7.30, base excess (BE) < −4 mEq/L and PaCO2 <= 45 mmHg. Main outcome measures: The primary outcome was the prevalence of metabolic acidosis. Secondary outcomes included ICU length of stay, hospital length of stay, receipt of renal replacement therapy (RRT), major adverse kidney events at 30 days (MAKE30), and hospital mortality. Results: Overall, 248 563 patients underwent analysis, with 11 537 (4.6%) in the Indigenous group and 237 026 (95.4%) in the non-Indigenous group. The prevalence of metabolic acidosis was higher in Indigenous patients (9.3% v 6.1%; P < 0.001). Indigenous patients with metabolic acidosis received RRT more often (28.2% v 22.0%; P < 0.001), but hospital mortality was similar between the groups (25.8% in Indigenous v 25.8% in non-Indigenous; P = 0.971). Conclusions: Critically ill Indigenous ICU patients are more likely to have a metabolic acidosis in the first 24 hours of their ICU admission, and more often received RRT during their ICU admission compared with non-Indigenous patients. However, hospital mortality was similar between the groups.