Obesity and its associated complications such as insulin resistance and non-alcoholic fatty liver disease are reaching epidemic proportions. In mice, the TGF-β superfamily is implicated in the regulation of white and brown adipose tissue differentiation. The kielin/chordin-like protein (KCP) is a secreted regulator of the TGF-β superfamily pathways that can inhibit both TGF-β and activin signals while enhancing bone morphogenetic protein (BMP) signaling. However, KCP's effects on metabolism and obesity have not been studied in animal models. Therefore, we examined the effects of KCP loss or gain of function in mice that were maintained on either a regular or a high-fat diet. KCP loss sensitized the mice to obesity and associated complications such as glucose intolerance and adipose tissue inflammation and fibrosis. In contrast, transgenic mice that expressed KCP in the kidney, liver, and adipose tissues were resistant to developing high-fat diet-induced obesity and had significantly reduced white adipose tissue. Moreover, KCP overexpression shifted the pattern of SMAD signaling , increasing the levels of phospho (P)-SMAD1 and decreasing P-SMAD3. Adipocytes in culture showed a cell-autonomous effect in response to added TGF-β1 or BMP7. Metabolic profiling indicated increased energy expenditure in KCP-overexpressing mice and reduced expenditure in the KCP mutants with no effect on food intake or activity. These findings demonstrate that shifting the TGF-β superfamily signaling with a secreted protein can alter the physiology and thermogenic properties of adipose tissue to reduce obesity even when mice are fed a high-fat diet.
We describe the case of a patient who had suspected myocardial ischemia, showed normal findings on multiple perfusion scans, and showed isolated cardiac sarcoidosis on 18 F-FDG-PET. Also discussed are the diagnosis and the monitoring of disease response using imaging follow-up.
Iatrogenic pulmonary vein stenosis (PVS) is a known, yet rare, complication of atrial radiofrequency ablation. Alterations in pulmonary perfusion may mimic massive pulmonary embolism on a ventilation/perfusion (V/Q) scintigraphy. This is particularly important due to the overlap in presenting clinical symptoms. The present case illustrates the functional significance of PVS and the changes in perfusion in response to angioplasty.
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