Assessment of virgin coconut oil in a balanced diet on indicators of cardiovascular health in non-obese volunteers: A human metabolic study.

BACKGROUND AND AIMS: Consumption of coconut oil is implicated in cardiovascular disease risk. On the contrary, virgin coconut oil (VCO) is believed to offer better health benefits, however, the evidence to support such claims is lacking, particularly in humans. Therefore, this study aimed at assessing the impact of VCO in a balanced diet on HDL-C and some of the anthropometric and biochemical parameters associated with human cardiovascular health before and after the feeding experiment. METHODS: In a crossover observational study, apparently healthy non-obese male volunteers (n = 22) aged between 28 and 50years with a mean body weight of 67.5 kg were inducted into a two-arm controlled feeding experiment one after another for eight weeks with a six-week washout period. In the first arm, the diets were prepared with VCO, whereas peanut oil was used in the second arm (∼35g/day) as the control. RESULTS: Compared to baseline, the consumption of VCO did not affect HDL-C and anthropometric measures at the end of the 8th week, whereas plasma total cholesterol (TC) and LDL-C levels (Means±standard error; 172 ± 5.6 mg/dL versus 186 ± 5.9 mg/dL and 113 ± 4.29 mg/dL versus 126 ± 4.17 mg/dL respectively) increased significantly. However, plasma triglycerides and some of the cardiovascular risk markers (namely, vascular cell-adhesion molecules, serum amyloid proteins and C-reactive protein) remained unaltered. Further, most of the changes in the VCO arm were comparable to the peanut oil regimen. CONCLUSION: The consumption of VCO in a balanced diet displayed neutral effects on most parameters related to cardiovascular risk. However, the rise in TC and LDL-C must be tested in a larger sample size over longer periods.

Coconut oil consumption improves fat-free mass, plasma HDL-cholesterol and insulin sensitivity in healthy men with normal BMI compared to peanut oil.

BACKGROUND & AIMS: The existing scientific evidence on coconut oil consumption and its health effects remains inconclusive due to varied reasons. In this context, we conducted a well-controlled metabolic study, eliminating some of the confounding factors and assessed the effects of the consumption of coconut oil-based diet on various anthropometric, biochemical and inflammatory markers and compared with peanut oil-diet. METHODS: Nine healthy male volunteers with BMI ≤25 kg/m2 were enrolled for this study and given balanced diets prepared with coconut oil (CO; ~35 g) for a period of eight weeks. After a wash-out period of six weeks, the same subjects were provided with diets prepared with peanut oil (~35 g) for eight weeks. Except fat source, the composition of the diets was identical in all aspects. RESULTS: Compared to basal values, there were significant increases in fat-free mass (p ≤ 0.022), plasma HDL-cholesterol (HDL-C) (p ≤ 0.047) and insulin sensitivity of the subjects at the end of CO-consumption. Further, compared to peanut oil, increase in plasma HDL-C was significant (p = 0.004) in CO treatment. On the other hand, plasma inflammatory markers-associated with cardiovascular diseases (CVD), namely soluble vascular cell adhesion molecule 1 (sVCAM1) and matrix metalloproteinase levels were reduced significantly by CO-intake. Further, these subjects displayed elevated levels of myristic acid (14:0) in plasma phospholipids at the end of CO-consumption, which correlated positively with HDL-C and negatively with sVCAM1. However, no such changes were observed after peanut oil diet consumption. CONCLUSIONS: In conclusion, compared to peanut oil, the consumption of coconut oil in a balanced diet resulted in increased fat-free mass, plasma HDL-C, elicited favourable changes on insulin sensitivity and CVD risk-associated parameters in healthy men with normal BMI.

Vitamin A deficiency increases the oleic acid (C18:1) levels in the kidney of high fructose diet-fed rats.

Background & objectives: Stearoyl-CoA desaturase 1 (SCD1) is a key lipogenic enzyme responsible for endogenous synthesis of monounsaturated fatty acids (MUFA) and plays a key role in various pathophysiology, including fatty liver diseases. In this experimental study the impact of vitamin A deficiency was assessed on SCD1 regulation in relation to kidney biology, under high fructose (HFr) diet-fed condition in rats. Methods: Forty male weanling (21 day old) Wistar rats were divided into four groups control, vitamin A-deficient (VAD), HFr, VAD with HFr consisting of eight rats each, except 16 for the VAD group. The groups received one of the following diets: control, VAD, HFr and VAD with HFr for 16 wk, except half of the VAD diet-fed rats were shifted to HFr diet, after eight week period. Results: Feeding of VAD diet (alone or with HFr) significantly reduced the kidney retinol (0.51, 0.44 µg/g vs. 2.1 µg/g; P < 0.05), while increased oleic (C18:1) and total MUFA levels (23.3, 22.2% and 27.3, 25.4% respectively vs. 14.7 and 16.6%; P < 0.05) without affecting the SCD1, both at protein and mRNA levels, when compared with HFr. Comparable, immunohistological staining for SCD1 was observed in the distal convoluted tubules. Despite an increase in MUFA, morphology, triglyceride content and markers of kidney function were not affected by VAD diet feeding. Interpretation & conclusions: Feeding of VAD diet either alone or under HFr condition increased the kidney oleic acid (C18:1) levels and thus total MUFA, which corroborated with elevated SCD1 activity index, without affecting its expression status. However, these changes did not alter the kidney morphology and function. Thus, nutrient-gene regulation in kidney biology seems to be divergent.

Development of Low Glycemic Index Foods and Their Glucose Response in Young Healthy Non-Diabetic Subjects.

Development of low glycemic-foods is important in the prevention and management of type 2 diabetes. In this context, we prepared four test foods (TFs) (two mixed mini-meals and two breakfast items) with low glycemic-components and assessed their glycemic index (GI) in young healthy non-diabetic volunteers with mean age of 29 yr, body mass index of 24 kg/m2, and fasting plasma glucose levels less than 4.62 mmol/L. Volunteers were given 50 g of glucose, as a reference food (RF) on the first day, and TFs, i.e. TF1 (mixed mini meal: roti made of wheat flour and chana dal+ curd), TF2 [mixed mini meal made of wheat, pearl barley, and Bengal gram flour (besan) mix with chana whole (unhusked chana+curd)], TF3 (pearl barley rawa upma), and TF4 (wheat rawa upma) were given 2-day intervals in the same order. Glucose levels at fasting conditions and after the consumption of RF and TFs at different time intervals (15, 30, 45, 60, 90, and 120 min) were measured, and the incremental area under curve (IAUC) for glucose and GI of the TFs were calculated. The glucose IAUC values at different time points were highest for TF2 (GI=71.9±7.4), while all other TFs had comparable GI in the range of 53.7~54.9. Among the various TFs, TF1, TF3, and TF4 exerted low to moderate glycemic response, and thus can be classified as low glycemic-foods. Nevertheless, these foods need to be tested for their efficacy in controlling and/or managing hyperglycemia and glucose over-load in diabetic subjects.

Carbenoxolone treatment ameliorated metabolic syndrome in WNIN/Ob obese rats, but induced severe fat loss and glucose intolerance in lean rats.

BACKGROUND: 11beta-hydroxysteroid dehydrogenase type 1 (11ß-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11ß-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11ß-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity. METHODOLOGY/PRINCIPAL FINDINGS: Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n = 6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11ß-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment. CONCLUSIONS/SIGNIFICANCE: We conclude that 11ß-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11ß-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11ß-HSD1 inhibition may lead to insulin resistance in normal conditions.

Dietary (n-3) long chain polyunsaturated fatty acids prevent sucrose-induced insulin resistance in rats.

This study was designed to determine the effect of substituting (n-3) long-chain PUFAs (LCPUFAs) for linoleic acid and hence decreasing the (n-6):(n-3) fatty acid ratio on sucrose-induced insulin resistance in rats. Weanling male Wistar rats were fed casein-based diets containing 100 g/kg fat for 12 wk. Insulin resistance was induced by replacing starch (ST) with sucrose (SU). The dietary fats were formulated with groundnut oil, palmolein, and fish oil to provide the following ratios of (n-6):(n-3) fatty acids: 210 (ST-210, SU-210), 50 (SU-50), 10 (SU-10), and 5 (SU-5). Compared with starch (ST-210), sucrose feeding (SU-210) significantly increased the plasma insulin and triglyceride concentrations and the plasma insulin area under the curve (AUC) in response to an oral glucose load. Adipocytes isolated from rats fed SU-210 had greater lipolytic rate, lower insulin stimulated glucose transport, and lower insulin-mediated antilipolysis than those from rats fed ST-210. Decreasing the dietary (n-6):(n-3) ratio in sucrose-fed rats (SU-10 and SU-5) normalized the plasma insulin concentration and the AUC of insulin after a glucose load. The sucrose-induced increase in plasma triglyceride concentration was normalized in rats fed SU-50, SU-10 and SU-5. Further, sucrose-induced alterations in adipocyte lipolysis and antilipolysis were partially reversed and glucose transport improved in rats fed diets SU-5 and SU-10. In diaphragm phospholipids, decreasing the (n-6):(n-3) ratio in the diet increased the concentration of (n-3) LCPUFAs with concomitant decreases in the concentration of (n-6) LCPUFAs. These results suggest that (n-3) LCPUFAs at a level of 2.6 g/kg diet [0.56% energy (n-3) LCPUFAs, (n-6):(n-3) ratio = 10] may prevent sucrose-induced insulin resistance by improving peripheral insulin sensitivity.