Purpose To investigate the effect of R2* modeling in conventional and accelerated measurements of skeletal muscle fat fraction in control subjects and patients with muscular dystrophy. Materials and Methods Eight patients with Becker muscular dystrophy and eight matched control subjects were recruited with approval from the Newcastle and North Tyneside 2 Research Ethics Committee and with written consent. Chemical-shift images with six widely spaced echo times (in 3.5-msec increments) were acquired to correlate R2* and muscle fat fraction. The effect of incorporating or neglecting R2* modeling on fat fraction magnitude and variance was evaluated in a typical three-echo protocol (with 0.78-msec increments). Accelerated acquisitions with this protocol with 3.65×, 4.94×, and 6.42× undersampling were reconstructed by using combined compressed sensing and parallel imaging and fat fraction maps produced with R2* modeling. Results Muscle R2* at 3.0 T (33-125 sec(-1)) depended on the morphology of fat replacement, the highest values occurring with the greatest interdigitation of fat. The inclusion of R2* modeling removed bias, which was greatest at low fat fraction, but did not increase variance. The 95% limits of agreement of the accelerated acquisitions were tight and not degraded by R2* modeling (1.65%, 1.95%, and 2.22% for 3.65×, 4.94×, and 6.42× acceleration, respectively). Conclusion Incorporating R2* modeling prevents systematic errors in muscle fat fraction by up to 3.5% without loss of precision and should be incorporated into all muscular dystrophy studies. Fat fraction measurements can be accelerated fivefold by using combined compressed sensing and parallel imaging, modeling for R2* without loss of fidelity.
The increased weight loss at 7 days following RYGB compared to 7 days of VLCD in T2DM is due to greater loss of lean and water mass After RYGB, the early and enhanced post-meal rise in glucose and insulin is due to rapid absorption through the gastroenterostomy The increased post-meal GLP-1 secretion specific to RYGB is not accompanied by an improvement in insulin or glucose AUC when compared to VLCD The early improvement in glucose control in T2DM after bariatric surgery is not explained by improved beta cell function The relationship between weight loss and loss of liver fat at 7 days following bariatric surgery and VLCD appears different 2
Abstract
AimsIt remains unclear whether the mechanism underlying the early improvement in glucose metabolism in type 2 diabetes following roux-en-Y gastric bypass surgery (RYGB) differs from that seen with a very low calorie diet (VLCD). Specifically, whether the markedly increased GLP-1 secretion following surgery is of primary importance has been controversial. This study compared directly the impact of GLP-1 secretion on glucose metabolism in individuals with type 2 diabetes listed for RYGB, randomised to be studied before and at 7 days following RYGB or VLCD.
MethodsA semi-solid meal test was used to investigate glucose, insulin and GLP-1 response. Insulin secretion to intravenous glucose and arginine stimulus was measured. Hepatic and pancreatic fat content was quantified using a magnetic resonance (MR) method.
ResultsDecrease in fat mass was almost identical after surgery or VLCD (3.0±0.3 and 3.0±0.7kg). The early plasma glucose rise and acute insulin secretion were greater following surgery than VLCD. However, the early GLP-1 rise was disproportionately greater (7-fold) after surgery than VLCD. This did not translate into a greater improvement in fasting glucose or glucose area under the curve. The reduction in liver fat was greater after surgery (29.8±3.7 vs. 18.6±4.0%) and the relationship between weight loss and reduction in liver fat differed following surgery or VLCD.
ConclusionsIn conclusion, this study demonstrates that gastroenterostomy increases the rate of nutrient absorption, bringing about a commensurately rapid rise insulin. However, there was no relationship with the large post-meal rise in GLP-1 and post-meal glucose homeostasis was similar after surgery or VLCD.
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