It is well known that troglitazone and voluntary running have the capacity to improve insulin resistance. The purpose of this study was to evaluate the combination effect of troglitazone and voluntary running on insulin action. Female rats aged 7 weeks were divided into high-fat diet (HF), high-fat diet + troglitazone (0.3% in diet; Tg), high-fat diet + voluntary running (for 3 wks; Tr), high-fat diet + troglitazone + voluntary running (Tg-Tr), and control (C) groups. A sequential euglycemic clamp experiment with two different insulin infusion rates of 3.0 (L-clamp) and 30.0 mU/kg BW/min (H-clamp) was performed on these rats after an overnight fast. Blood glucose concentrations were kept at fasting levels by periodic adjustment of the intravenous glucose infusion rate during the clamp experiment. Glucose infusion rates (GIRs) calculated from 60 to 90, 150 to 180 min were regarded as an index of whole body insulin action. After the clamp experiment, we determined the amount of glycogen content in the gastrocnemius muscle. Fat feeding markedly reduced GIRs in both L- and H- clamp experiments compared with C. Troglitazone treatment did not improve high-fat induced insulin resistance. In both L- and H-clamp experiments, GIRs were increased by voluntary running compared with HF, and reached the same levels as in C. GIRs of Tg-Tr were not greater than those of Tr. Glycogen content in gastrocnemius muscle showed the same trend as the results for GIRs. Therefore, the combination effect of troglitazone and voluntary running on insulin action was not found, but the effect of voluntary running was shown in fat-induced insulin resistance.
Early diagnosis of basilar artery occlusion (BAO) based only on clinical findings is challenging. We present a fully recovered case of BAO caused by pulmonary arteriovenous malformation (PAVM) that was diagnosed early using a protocol for CT angiography (CTA) and promptly treated with endovascular therapy (EVT). A woman in her 50s complained of vertigo with normal level of consciousness (LOC). On arrival, her LOC decreased to a Grass Coma Scale score of 12, and we performed a CT chest-cerebral angiography protocol. Head CTA showed BAO, and an intravenous tissue plasminogen activator was administered, followed by EVT. Chest contrast-enhanced CT showed PAVM in segment 10 of the left lung, which was treated with coil embolisation. For patients with a complaint of vertigo, BAO should be suspected, even if they have an initially normal LOC. A CT chest-cerebral angiography protocol is useful for prompt diagnosis and treatment of BAO and can reveal undetermined causes.
Brown adipose tissue (BAT) plays a crucial role in energy expenditure and is recognized as a therapeutic target in metabolic diseases. Chronic inflammation is a common etiology of obesity and type 2 diabetes. A previous study reported increased inflammation in BAT from obese animals. Regular exercise is an effective tool for improving obesity; however, it remains unclear whether exercise training affects the inflammation in BAT from obese animals. Purpose To examine the effects of exercise training on the activation of inflammation‐related signaling in BAT from obese/diabetic rats. Methods Male Otsuka Long‐Evans Tokushima Fatty (OLETF) rats, a rodent model for obesity/diabetes, were randomly assigned to either sedentary (n = 11) or exercise training (n = 8) groups. Long‐Evans Tokushima Otsuka (LETO; n = 9) rats were used as the non‐diabetic sedentary control. Exercise training on the treadmill was conducted 4 days/week for 20 weeks from 5 weeks of age. An intraperitoneal glucose tolerance test was performed and interscapular BAT was dissected, and phosphorylation levels of inflammatory‐related proteins, as well as the expression levels of mitochondrial proteins, were determined by western blot analysis. Results The phosphorylation levels of p65 (a subunit of NF‐κB) and mitogen‐activated protein kinases (MAPK; p38, ERK1/2, and SAPK/JNK) in the BAT were significantly higher in the sedentary OLETF rats when compared to those in the LETO rats. Exercise training attenuated the increase in the phosphorylation levels of NF‐κB and MAPKs in the BAT from the OLETF rats. Moreover, the expression levels of UCP‐1 and ‐3 and oxidative phosphorylation‐related proteins (NDUFB8, SDHB, UQCRC2, MTCO1 and ATP5A) in the BAT were significantly lower in the sedentary OLETF rats than the LETO rats, but exercise training did not alter this. Conclusion Exercise training prevents obesity‐induced activation of NF‐κB and MAPK signaling in BAT from obese/diabetic rats. Support or Funding Information This work was supported by grants from the MEXT‐Supported Program for the Strategic Research Foundation at Private Universities (S1101008) and a Grant‐in‐Aid for JSPS Fellows (13J10819).
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