Reductions in body weight and insulin resistance are not associated with changes in grey matter volume or cortical thickness during the PREVIEW study.

INTRODUCTION: The effect of changes in body weight or insulin resistance on grey matter volume and cortical thickness change are unclear. The present observational study assessed effects of an 8-week weight loss period (≥8% of body weight), and a subsequent 22-month weight maintenance period on grey matter volume and cortical thickness. METHODS: A total of 24 participants (12f/12 m; age 52.8 ±â€¯10.6 years) with overweight/obesity and pre-diabetes were recruited. T1-weighted magnetic resonance imaging was used to determine grey matter volume and cortical thickness at baseline, after the weight loss period and after a medium to high dietary protein weight maintenance period. RESULTS: At baseline, global grey matter volume was inversely associated with HOMA-IR, adjusted for sex and age (r = -0.42; p = .049). During the weight loss period participants decreased their BMI (32.1 ±â€¯3.3 to 28.1 ±â€¯2.8 kg/m2, p < .01), body-fat (41.6 ±â€¯6.4 to 35.0 ±â€¯8.0%, p < .01) and insulin resistance (HOMA-IR: 4.0 ±â€¯2.0 to 1.8 ±â€¯0.9, p < .01). During the 22-month weight maintenance period, these parameters gradually increased again (BMI: 29.3 ±â€¯3.8 kg/m2; body-fat: 37.8 ±â€¯9.3%; HOMA-IR: 2.9 ±â€¯1.4, p < .01). Global grey matter volume and cortical thickness did not change significantly during the weight loss or weight maintenance period. Changes in body weight, body-fat percentage or insulin sensitivity were not associated with changes in global grey matter volume. CONCLUSION: In conclusion, we confirmed that global grey brain matter volume was inversely associated with insulin resistance at baseline, yet an intervention yielding a decrease in insulin resistance did not lead to changes in global grey brain matter volume or cortical thickness. TRIAL REGISTRATION: The trial is registered with ClinicalTrials.gov, NCT01777893.

Long-term effects of increased protein intake after weight loss on intrahepatic lipid content and implications for insulin sensitivity: a PREVIEW study.

The aim of this study was to assess the effects of a weight maintenance period comprising two diets differing in protein intake, after weight loss, on intrahepatic lipid content and implications for insulin sensitivity. A total of 25 participants [body mass index (BMI): 31.1 (3.5 kg/m2; intrahepatic lipid (IHL): 8.7 (8.3%; fasting glucose: 6.4 (0.6 mmol/l; homeostatic model assessment for insulin resistance (HOMA-IR): 3.7 (1.6; Matsuda index: 3.4 (2.9] started an 8-wk low-energy diet followed by a 2-yr weight maintenance period with either high protein or medium protein dietary guidelines. At baseline, after 6 mo, and after 2 yr, IHL, visceral adipose tissue (VAT), and subcutaneous adipose tissue (SAT) were determined by magnetic resonance spectroscopy/imaging. Glucose and insulin concentrations, determined during an oral glucose challenge, were used to assess the HOMA-IR and Matsuda insulin sensitivity index (ISI). Protein intake was measured with 24-h urinary nitrogen excretion. Protein intake, BMI, IHL, VAT, SAT, HOMA-IR, and ISI did not change differently between the groups during the intervention. In the whole group, BMI, IHL, VAT, SAT, HOMA-IR, and ISI were favorably changed at 6 mo and 2 yr compared with baseline ( P < 0.05). Mixed-model analysis showed that independent of BMI, protein intake (g/d) at 6 mo was inversely related to IHL (coefficient: -0.04; P < 0.05) and VAT (coefficient: -0.01; P < 0.05). Overall, IHL was positively related to HOMA-IR (coefficient: 0.10; P < 0.01) and inversely related to ISI (coefficient: -0.17; P < 0.01), independent of BMI. A 2-yr medium- to high-protein energy-restricted diet reduced IHL and VAT. Independently of changes in BMI, IHL was inversely related to insulin sensitivity.

In vivo molecular imaging of apoptosis and necrosis in atherosclerotic plaques using microSPECT-CT and microPET-CT imaging.

PURPOSE: The purpose of this paper is to study molecular imaging of apoptosis and necrosis, two key players in atherosclerosis instability, using a multimodal imaging approach combining single photon emission computed tomography (SPECT), positron emission tomography (PET), and computed tomography (CT). PROCEDURES: Collar-induced carotid atherosclerosis ApoE knockout mice were imaged with (99m)Tc-AnxAF568 SPECT-CT to study apoptosis and sequentially with PET-CT following (124)I-Hypericin ((124)I-Hyp) injection to visualize necrosis. RESULTS: SPECT depicted increased (99m)Tc-AnxAF568 uptake in both atherosclerotic carotid arteries, whereas our data suggest that this uptake is not merely apoptosis related. Although PET of (124)I-Hyp was hampered by the slow blood clearance in atherosclerotic mice, (124)I-Hyp was able to target necrosis in the atherosclerotic plaque. CONCLUSION: Both (99m)Tc-AnxAF568 and (124)I-Hyp uptake are increased in atherosclerotic carotid vasculature compared to control arteries. While apoptosis imaging remains challenging, necrosis imaging can be feasible after improving the biodistribution characteristics of the probe.