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Aim: To investigate the incretin axis in people with cystic fibrosis. Methods: Adults with cystic fibrosis‐related diabetes, cystic fibrosis without diabetes, and controls (adults without cystic fibrosis and without diabetes) underwent an oral glucose tolerance test and then a closely matched isoglycaemic i.v. glucose infusion. On each occasion, glucose, insulin, C‐peptide, total and active glucagon‐like peptide‐1 and gastric inhibitory polypeptide responses were recorded and incremental areas under curves were calculated for 60 and 240 min. Results: Five adults with cystic fibrosis‐related diabetes, six with cystic fibrosis without diabetes and six controls, matched for age and BMI, completed the study. Glucose during oral glucose tolerance test closely matched those during isoglycaemic i.v. glucose infusion. The calculated incretin effect was similar in the control group and the cystic fibrosis without diabetes group (28% and 29%, respectively), but was lost in the cystic fibrosis‐related diabetes group (cystic fibrosis‐related diabetes vs control group: –6% vs 28%; p=0.03). No hyposecretion of glucagon‐like peptide‐1 or gastric inhibitory polypeptide was observed; conversely, 60‐min incremental area under the curve for total glucagon‐like peptide‐1 was significantly higher in the cystic fibrosis‐related diabetes group than in the control group [1070.4 (254.7) vs 694.97 (308.1); p=0.03] Conclusions: The incretin effect was lost in cystic fibrosis‐related diabetes despite adequate secretion of the incretin hormones. These data support the concept that reduced incretin hormone insulinotropic activity contributes significantly to postprandial hyperglycaemia in cystic fibrosis‐related diabetes. What's new?: This study is the first to measure the incretin effect in people with cystic fibrosis (CF).The incretin effect is lost in people with cystic fibrosis‐related diabetes (CFRD) despite adequate secretion of glucagon‐like peptide‐1 and gastric inhibitory polypeptide.In people with CF but not diabetes, the incretin effect is similar to that in people without CF.These data suggest the lack of incretin effect contributes to postprandial hyperglycaemia, a hallmark of CFRD, most likely as a consequence of reduced β‐cell mass. [ABSTRACT FROM AUTHOR]

Osteoarthritis is the leading musculoskeletal cause of disability in the Western society. Despite this, it is still difficult to gain a precise definition of what osteoarthritis actually is. The methods used for the study are narrative review and viewpoint focussing on the knee. It is well known that there is a modest correlation between X-ray changes and pain. Improvements in imaging have shown that osteoarthritis should be regarded as an umbrella term for a number of pathophysiological processes leading to pain and/or cartilage loss. If these are inside the joint (such as bone marrow lesions, cartilage defects or meniscal tear) then they can be considered osteoarthritis, while those outside the joint (such as obesity, weak muscles and vitamin D deficiency) could be considered the osteoarthritis syndrome. These improvements in basic science are leading to lesion-specific therapies indicating the importance of trying to pinpoint causes of pain in the individual. [ABSTRACT FROM AUTHOR]

Aims It has been proposed that the Chronic Kidney Disease Epidemiology Collaboration formula estimates glomerular filtration rate more accurately than the Modification of Diet in Renal Disease formula. With the very high incidence of diabetes and end-stage kidney disease in Indigenous Australians, accurate estimation of glomerular filtration rate is vital in early detection of kidney disease. We aimed to assess the performance of the Chronic Kidney Disease Epidemiology Collaboration, Modification of Diet in Renal Disease and Cockcroft-Gault formulas in Indigenous Australians with and without diabetes. Methods Indigenous Australians with ( n = 224) or without ( n = 340) Type 2 diabetes had a reference glomerular filtration rate measure using plasma disappearance of iohexol (measured glomerular filtration rate) over 4 h. Serum creatinine was measured by an enzymatic method. Performance was assessed by bias (measured glomerular filtration rate - estimated glomerular filtration rate) and accuracy (percentage of estimated glomerular filtration rate within 30% of measured glomerular filtration rate). Results The median measured glomerular filtration rate (interquartile range) in participants with or without diabetes was 97 (68-119) and 108 (90-122) ml min−1 1.73 m−2, respectively. The Chronic Kidney Disease Epidemiology Collaboration formula had smaller bias and greater accuracy than the Modification of Diet in Renal Disease and Cockcroft-Gault formulas overall, for participants both with and without diabetes. However, for estimated glomerular filtration rate > 90 ml min−1 1.73 m−2, the Chronic Kidney Disease Epidemiology Collaboration formula had greater bias in participants with diabetes, underestimating measured glomerular filtration rate by 7.4 vs. 1.0 ml min−1 1.73 m−2 in those without diabetes. The Chronic Kidney Disease Epidemiology Collaboration formula was less accurate across the whole range of estimated glomerular filtration rates in participants with vs. those without diabetes (87.1% vs. 93.3%). Conclusions The Chronic Kidney Disease Epidemiology Collaboration formula outperforms the Modification of Diet in Renal Disease and Cockcroft-Gault formulas overall in Indigenous Australians with and without diabetes. However, the Chronic Kidney Disease Epidemiology Collaboration formula has greater bias in people with diabetes compared with those without diabetes, especially in those with normal renal function. [ABSTRACT FROM AUTHOR]

Objective Foot pain is a common complaint in adults. Increased BMI and fat mass have been linked only to foot pain prevalence. Therefore, a longitudinal study to examine the relationship between body composition and incident foot pain over 3 years was conducted. Design and Methods Sixty-one community dwelling participants from a previous study of musculoskeletal health, who did not have foot pain at study inception in 2008, were invited to take part in this follow-up study in 2011. Current foot pain was determined using the Manchester Foot Pain and Disability Index, and body composition was measured using dual X-ray absorptiometry at study baseline. Results Of the 51 respondents (84% response rate, 37 females and 14 males), there were 11 who developed foot pain. BMI ranged from underweight to morbidly obese (17-44 kg/m2), mean 27.0 ± 6.0 kg/m2. Incident foot pain was positively associated with both fat mass (odds ratio [OR] 1.11, 95% confidence interval [CI] 1.03-1.20) and fat-mass index (OR 1.28, 95% CI 1.04-1.57) in multivariate analysis. Conclusions Fat mass is a predictor of incident foot pain. This study supports the notion that incident foot pain in overweight individuals is associated with fat mass rather than body mass alone. [ABSTRACT FROM AUTHOR]

Background: There is controversy about whether pain and radiographic osteoarthritis (ROA) predict subsequent cartilage loss. The aim of this study was to describe the relationship between ROA, pain and cartilage loss in the knee. Methods: We studied randomly selected subjects at baseline and approximately 2.9 years later ( n= 399). The presence of ROA was assessed at baseline with a standing anteroposterior semiflexed radiograph scored using the Osteoarthritis Research Society International atlas for osteophytes (OP) and joint space narrowing (JSN). Pain was assessed by the Western Ontario McMaster Osteoarthritis Index. Subjects' medial and lateral tibial cartilage volumes were determined by magnetic resonance imaging at both time points. Results: In cross-sectional analysis, both medial and lateral tibial cartilage volumes were lower in those with ROA. Any medial ROA predicted medial tibial cartilage loss (3.2% (standard deviation (SD) 5.6) vs 1.9% (SD 5.3) per annum) while any lateral ROA predicted both medial (4.0% (SD 6.0) vs 2.2% (SD 5.3) per annum) and lateral (3.5% (SD 5.8) vs 1.6% (SD 4.2) per annum) tibial cartilage loss (all P < 0.05). In multivariate analysis, JSN and OP at both medial and lateral sites had independent dose-response associations with tibial cartilage loss at both sites. Pain was an independent predictor of lateral, but not medial, tibial cartilage loss after taking ROA into account. Conclusions: Subjects with ROA (either JSN or OP) and, to a lesser extent, pain lose cartilage faster than subjects without ROA and the more severe the ROA the greater the rate of loss. These findings have implications for the design of clinical trials. [ABSTRACT FROM AUTHOR]