Adipose tissue is an active endocrine organ, and our knowledge of this secretory tissue, in recent years, has led us to completely rethink how our body functions and becomes dysregulated with weight gain. Human adipose tissue appears to act as a multifunctional secretory organ with the capacity to control energy homoeostasis through peripheral and central regulation of energy homoeostasis. It also plays an important role in innate immunity. However, the capability to more than double its original mass to cope with positive energy balance in obesity leads to many pathogenic changes. These changes arise within the adipose tissue as well as inducing secondary detrimental effects on other organs like muscle and liver, including chronic low-grade inflammation mediated by adipocytokines (adipokine inflammation). This inflammation is modulated by dietary factors and nutrients including glucose and lipids, as well as gut bacteria in the form of endotoxin or LPS. The aim of this current review is to consider the impact of nutrients such as glucose and lipids on inflammatory pathways, specifically within adipose tissue. Furthermore, how nutrients such as these can influence adipokine inflammation and consequently insulin resistance directly through their effects on secretion of adipocytokines (TNFα, IL6 and resistin) as well as indirectly through increases in endotoxin is discussed.

Peripheral action of irisin improves glucose homeostasis and increases energy expenditure, with no data on a central role of irisin in metabolism. These studies sought to examine 1) presence of irisin in human cerebrospinal fluid (CSF) and banked human hypothalamic tissue, 2) serum irisin in maternal subjects across varying adiposities with or without gestational diabetes (GDM), and 3) their respective neonate offspring. CSF, serum, and neonatal cord serum were collected from 91 pregnant women with and without GDM attending for an elective cesarean section [body mass index (BMI): 37.7 ± 7.6 kg/m²; age: 32 ± 8.3 yr]. Irisin was assessed by ELISA and correlated with biochemical and anthropometric data. Irisin expression was examined in human hypothalamus by immunohistochemical staining. Serum irisin in pregnant women was significantly lower in nonobese compared with obese and GDM subjects, after adjusting for BMI, lipids, and glucose. Irisin was present in neonatal cord serum (237 ± 8 ng/ml) and maternal CSF (32 ± 1.5 ng/ml). CSF irisin correlated positively with serum irisin levels from nonobese and obese pregnant women ( P < 0.01), with CSF irisin significantly raised in GDM subjects ( P < 0.05). Irisin was present in human hypothalamic sections in the paraventricular neurons, colocalized with neuropeptide Y. Irisin was detectable in CSF and in paraventricular neurons. Maternal serum irisin was lower in nonobese pregnant women after adjusting for BMI and a number of metabolic parameters. These studies indicate that irisin may have a central role in metabolism in addition to the known peripheral role. Further studies investigating the central action of irisin in human metabolic disease are required.

OBJECTIVE Diabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD). Obstructive sleep apnea (OSA) is common in type 2 diabetes and increases oxidative stress. Hence, OSA could promote the development and progression of DN. RESEARCH DESIGN AND METHODS This was a cohort study in adults with type 2 diabetes. Patients with known OSA or ESRD were excluded. DN was defined as the presence of albuminuria or an estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m². DN progression was based on eGFR measurements. OSA was defined as apnea hypopnea index (AHI) ≥5 events/h. Serum nitrotyrosine abundance (a marker of nitrosative stress) was measured by ELISA. RESULTS A total of 224 patients were included. OSA and DN prevalence was 64.3 and 40.2, respectively. DN prevalence was higher in patients with OSA (OSA⁺) compared with those without OSA (OSA⁻) (49.3% vs. 23.8%, P < 0.001). After adjustment, OSA (odds ratio 2.64 [95% CI 1.13–6.16], P = 0.02) remained independently associated with DN. After an average follow-up of 2.5 (0.7) years, eGFR decline was greater in OSA⁺ compared with OSA⁻ patients (median −6.8% [interquartile range −16.1 to 2.2] vs. −1.6% [−7.7 to 5.3%], P = 0.002). After adjusting, both baseline OSA (B = −3.8, P = 0.044) and AHI (B = −4.6, P = 0.02) remained independent predictors of study-end eGFR. Baseline serum nitrotyrosine abundance (B = −0.24, P = 0.015) was an independent predictor of study-end eGFR after adjustment. CONCLUSIONS OSA is independently associated with DN in type 2 diabetes. eGFR declined faster in patients with OSA. Nitrosative stress may provide a pathogenetic link between OSA and DN. Interventional studies assessing the impact of OSA treatment on DN are needed.

Introduction: The prevalence of eating disorders is high in people with higher weight. However, despite this, eating disorders experienced by people with higher weight have been consistently under-recognised and under-treated, and there is little to guide clinicians in the management of eating disorders in this population.Aim: The aim of this guideline is to synthesise the current best practice approaches to the management of eating disorders in people with higher weight and make evidence-based clinical practice recommendations.Methods: The National Eating Disorders Collaboration Steering Committee auspiced a Development Group for a Clinical Practice Guideline for the treatment of eating disorders for people with higher weight. The Development Group followed the ‘Guidelines for Guidelines’ process outlined by the National Health and Medical Research Council and aim to meet their Standards to be: 1. relevant and useful for decision making; 2. transparent; 3. overseen by a guideline development group; 4. identifying and managing conflicts of interest; 5. focused on health and related outcomes; 6. evidence informed; 7. making actionable recommendations; 8. up-to-date; and, 9. accessible. The development group included people with clinical and/or academic expertise and/or lived experience. The guideline has undergone extensive peer review and consultation over an 18-month period involving reviews by key stakeholders, including experts and organisations with clinical academic and/or lived experience.Recommendations: Twenty-one clinical recommendations are made and graded according to the National Health and Medical Research Council evidence levels. Strong recommendations were supported for psychological treatment as a first-line treatment approach adults (with bulimia nervosa or binge-eating disorder), adolescents and children. Clinical considerations such as weight stigma, interprofessional collaborative practice and cultural considerations are also discussed.Conclusions: This guideline will fill an important gap in the need to better understand and care for people experiencing eating disorders who also have higher weight. This guideline acknowledges deficits in knowledge and consequently the reliance on consensus and lower levels of evidence for many recommendations, and the need for research particularly evaluating weight-neutral and other more recent approaches in this field.