Dietary supplementation of mustard oil reduces blood glucose levels by triggering insulin receptor signaling pathway

Background Dietary fatty acids can alter membrane fatty acid composition with the consequent change in the action of various receptors. Incorporation of mustard oil was found to increase insulin secretion, reduce blood glucose levels, and increase the expression of glucose transporter gene 4 ( Glut4 ). Methods Three-week-old male Wistar rats were fed with 8% lipid-inclusive isocaloric mash diet. There were non-diabetic control (NDC) and diabetic control (DC) groups fed with ghee, and similarly non-diabetic (NDT) and diabetic treatment (DT) groups fed with mustard oil. Streptozotocin (STZ) was administered intraperitoneally once at a dose rate of 40 mg/kg bodyweight for the induction of diabetes. Blood glucose was estimated using glucometer periodically. Lipids were extracted from mustard oil and in tissue samples, and fatty acid estimation was done using gas chromatography (GC). Gene expression of 84 genes related to diabetes was measured in muscle tissue using Qiagen™ RT 2 polymerase chain reaction (PCR) profiler array. The real-time PCR data obtained as threshold cycle (Ct) values were analyzed using Ingenuity Pathway Analysis ® (IPA®) software. Results After induction of diabetes by day 30, the average glucose levels were above 500 mg/dL in diabetic groups, but for the mustard oil treatment group, they were reduced to 337 mg/dL by the 60 days of treatment. Significantly higher levels of unsaturated fatty acids particularly linoleic acid and linolenic acid were found in mustard oil treatment groups. Insulin receptor signaling was prominent in both ghee-fed normal and mustard oil–fed diabetic treatment groups. Glucose was found to be the major upstream regulator in all the groups except for ghee-fed diabetic control group. Conclusions Mustard oil inclusion in the diet reduces blood glucose levels by increased insulin receptor signaling, thereby partially reversing diabetic state in experimentally induced diabetic rats.