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Two new indexes of DI and BCF, parallel to HOMA basal indexes, based on analysis of 1313 individuals subjected to 75 Gm OGTT are proposed. Glucose and insulin Area Under Curve (AUC) values were calculated using trapezoidal rule. OGTT Insulin Secretion (Isec) was calculated using ’AUCins/AUCglu’ and insulin sensitivity (Isen) by using ’(1/(AUCins * AUCglu)’ formula which was derived by omitting basal values from Matsuda Index. Calculation of Disposition Index (OGTT-DI) i.e., ISec*ISen, was found proportional to ’1/(AUCglu)^2’, as the ’AUCins’ values in denominator and numerator were cross-cancelled. Considering other non-insulin dependent glucose disposal variables as ’constant’, a new index of BCF function, OGTT-B, was defined and derived using ’(OGTT-DI Test/OGTT-DI Normal) * 100’ formula. This resulted in a final equation as ’[{(AUCglu normal) ^2/(AUCglu-test) ^2} * 100]’. Normal AUCglu, a population specific variable, was determined from 10 normoglycemic non-obese individuals and was ’241’. Fourteen categories of dysglycemia were defined based on glucose, insulin, HOMA-IR and Matsuda index. When compared, OGTT-DI showed more consistent linear relationship to evolving dysglycemia categories than other BCF indexes such as HOMA-DI, oral-DI and ISSI-2. (Figure below). Being independent of Insulin and BMI levels, OGTT-DI and OGTT-B are simple and low cost BCF indexes which will be useful in staging and managing dysglycemia. Disclosure S.N. Shinde: None. R.S. Shinde: None. A.S. Joshi: None.

OGTT can be used to calculate various indexes of insulin secretion, resistance and beta cell function and to stratify the dysglycemic stage. Since calculating these indexes involves complex mathematical calculations, they are less commonly used. Realizing this, we created a single page web-based computer application to calculate these OGTT indexes. The values obtained during standard 75 gm, two-hour OGTT were entered in an Excel worksheet using standard formulas. This was then converted into a web-based calculator. The app can be used on all platforms and devices including smartphones. Once downloaded into a browser, the user needs to replace the default values with patient values obtained during OGTT. The app calculates and prints fasting, post glucose indexes and generates graphical charts showing the comparison between the patient and the expected normal values. It can email a copy for record and works in offline mode also. This app is in public domain and can be freely downloaded from www.ogtt.in. Even though less sensitive, HOMA indexes are commonly used due to their simple formulas. This calculator makes it very easy to calculate the post-glucose indexes which help in early recognition of specific organ resistance and clinical conditions such as obesity, prediabetes, fatty liver, PCOS, gestational diabetes, T2DM. Clinicians can use this rapid and easy tool for risk stratification of dysglycemia and to assess the response to therapy. Disclosure S.N. Shinde: None. A.S. Joshi: None. R.S. Shinde: None.

Insulin and glucose parabolas of OGTT were studied in 1030 subjects, not previously diagnosed as having T2DM. The parabola shape was mainly influenced by adiposity, peripheral Insulin resistance (PIR), beta cell(BC) mass and glucose dose. Fasting hyperinsulinemia(HI) was strongly related to body mass index(BMI). Continued calorie excess(CCE) and BMI along with increase in insulin area under curve, which suggested recruitment of new insulin receptors, acted as BC stressor leading to HI. Fasting HI appears to be a physiological response to incremental BMI, independent of PIR. The rate of rise of insulin (RIR) sustained an angle theta with baseline and both were related to BMI and PIR. The RIR was directly related to rising BMI, fasting insulin and glucose but was inversely related to PIR, 120 min insulin and glucose. CCE affected the Degree of HI whereas PIR affected the Duration of HI (Fig 1). From NoDM category as CCE begins, RIR and theta increase until PIR becomes unmasked. RIR, which is related to PIR, can not rise further. As CCE continues, at variable maximum level of insulin, the individual’s BC capacity, betamax, is reached. The RIR and theta start falling hereafter, until the final values for DM category. Gene-Calorie hypothesis proposes that PIR is an inherited predisposing factor where as CCE with adiposity is an acquired precipitating factor which together cause continuous BC stress and subsequent BC failure leading to T2DM. Disclosure S.N. Shinde: Advisory Panel; Self; USV Private Limited, Alkem Laboratories, Lupin Laboratories, Troikka Ltd, IPCA laboratories. R.S. Shinde: None.

The electrocardiogram of a patient with acute pulmonary embolism showed right bundle branch block (RBBB) on alternate beats; following thrombolysis, the pattern evolved to persistent RBBB and eventually to normal conduction. Analysis of serial tracings suggested that the mechanism of RBBB alternans was tachycardia-dependent bidirectional bundle branch block, caused by prolongation of both anterograde and retrograde refractory periods (RPs) of the right bundle branch (RBB). The sinus impulse found the RBB refractory, and was conducted over the left bundle branch only, depolarizing the left ventricle and then attempting to penetrate retrogradely the RBB; at that time, however, the RBB was still refractory. When a QRS complex had a RBBB configuration, therefore, the RBB was not depolarized; the ensuing sinus impulse found the RBB fully responsive as a consequence of the long period intervening between two successive depolarizations, and resulted in normal intraventricular conduction. With right ventricular afterload decrease, the recovery of RBB anterograde and retrograde excitability was asynchronous, since the retrograde RP became normal earlier than the anterograde one. In accordance with the relatively short retrograde RP, the RBB was retrogradely invaded by the transseptal impulse coming from the left ventricle; this "shifted to the right" the anterograde RP of the RBB. The RBB, thus, was still refractory to the next sinus impulse, and RBBB again occurred; the RBB, thus, was once more depolarized retrogradely, and this led to perpetuation of RBBB. Finally, intraventricular conduction became normal owing to full normalization of RBB anterograde and retrograde refractoriness.

The effects of the administration of coenzyme Q10 (3 mg/kg per day) (group A, n=10) and placebo (aluminum hydroxide, 3 mg/kg per day) (group B, n=10) were compared over 24 weeks in a randomized, single-blind, controlled trial. There were two groups of rabbits receiving a trans fatty acid (TFA)-rich diet (5-8 g/day) for 36 weeks. Oxidized rabbit chow with vitamin C plus ferric chloride was administered for 4 weeks in all rabbits. Intervention with coenzyme Q10 after feeding of TFA-rich diet was associated with a significant decline in thiobarbituric acid reactive substances (TBARS), diene conjugates and malondialdehyde, and an increase in plasma levels of vitamin E in the coenzyme Q group compared to placebo group. These changes, which were indicators of a decrease in oxidative damage, were independent of lipid lowering. The aortic and coronary artery plaque sizes, coronary atherosclerosis index, aortic and coronary atherosclerosis scores were significantly lower in the coenzyme Q group than placebo group. Aortic and coronary plaque frequencies, as well as frequencies of ulceration, thrombosis or hemorrhage, and cracks and fissures, were also significantly lower in the coenzyme Q group, indicating a better quality of atheroma compared to those in the control group. Aortic cholesterol, triglycerides and sudanophilia were significantly lower and vitamin E significantly higher in the coenzyme Q group in comparison to the placebo group indicating that coenzyme Q10 can have beneficial effect on the chemical composition of atheroma. The findings suggest that antioxidant therapy with coenzyme Q10 may be used as an adjunct to lipid lowering for additional beneficial effects related to chemical composition and quality of atheroma independent of hypolipidemic agents.