Background: Information on anatomical connectivity in the brain by measurements of the diffusion of water in white matter tracts lead to quantification of local tract directionality and integrity.

Background: While adiposity is a well-established risk factor for cardiovascular disease, the association between adiposity and cerebrovascular disease is not entirely understood. For example, common methods to quantify body fat volume such as body mass index, waist circumference and waist-to-hip ratio are not suitable to identify the complex distribution patterns of body fat and its relation to cerebrovascular pathology. In view of a better understanding of the association between fat distribution and cerebrovascular disorders, the aim of the study was to perform measurements of body fat distribution patterns and body fat volumes in correlation to arteriosclerosis of the brain-feeding arteries and white matter lesion load (WMLL). Methods: In this study we performed a magnetic resonance imaging (MRI)-based volumetric differential analysis of subcutaneous and visceral body fat distribution in 25 patients with MRI-proven hyperacute ischemic stroke. For the measurement of adipose tissue volume and tissue distribution automatic labeling analysis software was used. A correlation analysis of MRI volumetric measurements of subcutaneous and visceral body fat, atherosclerotic plaque load of the brain-feeding arteries measured by computed tomography angiography, and WMLL measured by MRI volumetry of the whole brain was performed. Results: The normalized total abdominal adipose tissue and the normalized subcutaneous abdominal adipose tissue showed no significant correlation with either WMLL or total plaque volume. In contrast, the normalized visceral adipose tissue showed a significant correlation with WMLL volume. Visceral adipose tissue as a percentage of total adipose tissue showed a significant correlation with WMLL. In particular, the percentage of visceral adipose tissue rather than total body fat volume strongly correlated with atherosclerosis and ischemic cerebral lesions. Furthermore, the volume of both soft and calcified plaques correlated significantly with WMLL. Conclusions: Our results contribute to existing studies about the association of different patterns of fat distribution with atherosclerosis of the brain-feeding arteries, in particular highlighting the importance of visceral adiposity as a risk factor for cerebrovascular disease. The percentage of visceral adipose tissue in total adipose tissue has the potential of a sensitive parameter and might become a relevant new epidemiological marker, showing highly significant correlations with well-established markers of cerebrovascular disease. In conclusion, the percentage of visceral adipose tissue by itself has to be regarded as a risk factor for both small vessel cerebrovascular disease and cerebral atherosclerosis of the large-to-medium-sized arteries.

Hobbs et al. p2 Characters in title = 95/96; words in abstract = 250/250; words in Introduction = 248/250; words in main text = 3235/3000; references = 25/40; Tables = 2; Figures = 2; Supplemental data = Methods, Results (4 Tables, 1 Figure), Strobe Checklist. Search Terms

The effects of linagliptin on fat content in diet-induced obese rats were compared with those of the appetite suppressant sibutramine. Female Wistar rats fed a high-fat diet (HFD) for 3 months received vehicle, linagliptin (10 mg/kg) or sibutramine (5 mg/kg) treatment orally, once daily for 6 additional weeks, while continuing the HFD. Magnetic resonance spectroscopy analysis of fat content was performed at baseline and at the end of the 6-week treatment period. Linagliptin treatment profoundly reduced hepatic fat compared with vehicle, with an effect comparable to that of sibutramine. The vehicle-corrected mean change (95% CI) from baseline in hepatic fat and intramyocellular lipid was -59.0% (-104.3%, -13.6%; p = 0.015) and -62.1% (-131.6%, 7.4%; p = 0.073), respectively, for linagliptin compared with -54.3% (-101.5%, -7.1%; p = 0.027) and -72.4% (-142.4%, -2.4%; p = 0.044), respectively, for sibutramine.

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