Postprandial Plasma Lipid Research Articles

Sex-Based Differences in Clinical Profile and Complications among Individuals with Type 2 Diabetes Seen at a Private Tertiary Diabetes Care Centre in India.

This study aimed to compare the clinical and biochemical profiles as well as the complications in males and females with type 2 diabetes (T2DM) presenting to a private tertiary diabetes care centre in India. This is a retrospective study, conducted between 1 January 2017 and 31 December 2019, and included 72,980 individuals with T2DM, aged ≥ 18 years (age and sex-matched-males-36,490; females-36,490). Anthropometric measurements, blood pressure, fasting plasma glucose (FPG), post-prandial plasma glucose (PPPG), glycated haemoglobin (HbA1c), lipids, urea, and creatinine were measured. Retinopathy was screened using retinal photography, neuropathy using biothesiometry, nephropathy measuring urinary albumin excretion, peripheral vascular disease (PVD) using Doppler, and coronary artery disease (CAD) based on the history of myocardial infarction and/or drug treatment for CAD and/or electrocardiographic changes. Obesity (73.6% vs. 59.0%) rates were significantly higher in females compared to males. FPG, PPPG, and HbA1c were higher among younger age groups among both sexes, with males having higher values compared to females. However, after the age of 44 years, control of diabetes was worse among females. In addition, only 18.8% of the females achieved glycemic control (HbA1c < 7%) compared to 19.9% in males (p < 0.001). Males had higher prevalence of neuropathy (42.9% vs. 36.9%), retinopathy (36.0% vs. 26.3%), and nephropathy (25.0% vs. 23.3%) compared to females. Males had 1.8- and 1.6-times higher risk of developing CAD and retinopathy compared to females. Hypothyroidism (12.5% vs. 3.5%) and cancers (1.3% vs. 0.6%) were significantly higher in females compared to males. In this large sample of T2DM seen at a chain of private tertiary diabetes centres, females had higher prevalence of metabolic risk factors and poorer diabetes control compared to males, emphasizing the need for better control of diabetes in females. However, males had higher prevalence of neuropathy, retinopathy, nephropathy, and CAD compared to females.

Low-fat dairy consumption improves intestinal immune function more than high-fat dairy in a diet-induced swine model of insulin resistance.

To understand the effects of consuming high-fat and low-fat dairy products on postprandial cardiometabolic risk factors and intestinal immune function, we used an established low birthweight (LBW) swine model of diet-induced insulin resistance. LBW piglets were randomized to consume one of the 3 experimental high fat diets and were fed for a total of 7weeks: (1) Control high fat (LBW-CHF), (2) CHF diet supplemented with 3 servings of high-fat dairy (LBW-HFDairy) and (3) CHF diet supplemented with 3 servings of low-fat dairy (LBW-LFDairy). As comparison groups, normal birthweight (NBW) piglets were fed a CHF (NBW-CHF) or standard pig grower diet (NBW-Chow). At 11weeks of age, all piglets underwent an established modified oral glucose and fat tolerance test. At 12weeks of age, piglets were euthanized and ex vivo cytokine production by cells isolated from mesenteric lymph node (MLN) stimulated with mitogens was assessed. Dairy consumption did not modulate postprandial plasma lipid, inflammatory markers and glucose concentrations. A lower production of IL-2 and TNF-α after pokeweed mitogen (PWM) stimulation was observed in LBW-CHF vs NBW-Chow (P < 0.05), suggesting impaired MLN T cell function. While feeding high-fat dairy had minimal effects, feeding low-fat dairy significantly improved the production of IL-2 and TNF-α after PWM stimulation (P < 0.05). Irrespective of fat content, dairy had a neutral effect on postprandial cardiometabolic risk factors. Low-fat dairy products improved intestinal T cell function to a greater extent than high-fat dairy in this swine model of obesity and insulin resistance.

GLP-1 attenuates intestinal fat absorption and chylomicron production via vagal afferent nerves originating in the portal vein

Background/ObjectiveGLP-1R agonists have been shown to reduce fasting and postprandial plasma lipids, both of which are independent risk factors for the development of cardiovascular disease. However, how endogenous GLP-1 – which is rapidly degraded – modulates intestinal and hepatic lipid metabolism is less clear. A vagal gut-brain-axis originating in the portal vein has been proposed as a possible mechanism for GLP-1’s anti-lipemic effects. Here we sought to examine the relationship between vagal GLP-1 signalling and intestinal lipid absorption and lipoprotein production. MethodsSyrian golden hamsters or C57BL/6 mice received portal vein injections of GLP-1(7-36), and postprandial and fasting plasma TG, TRL TG, or VLDL TG were examined. These experiments were repeated during sympathetic blockade, and under a variety of pharmacological or surgical deafferentation techniques. In addition, hamsters received nodose ganglia injections of a GLP-1R agonist or antagonist to further probe the vagal pathway. Peripheral studies were repeated in a novel GLP-1R KO hamster model and in our diet-induced hamster models of insulin resistance. ResultsGLP-1(7-36) site-specifically reduced postprandial and fasting plasma lipids in both hamsters and mice. These inhibitory effects of GLP-1 were investigated via pharmacological and surgical denervation experiments and found to be dependent on intact afferent vagal signalling cascades and efferent changes in sympathetic tone. Furthermore, GLP-1R agonism in the nodose ganglia resulted in markedly reduced postprandial plasma TG and TRL TG, and fasting VLDL TG and this nodose GLP-1R activity was essential for portal GLP-1s effect. Notably, portal and nodose ganglia GLP-1 effects were lost in GLP-1R KO hamsters and following diet-induced insulin resistance. ConclusionOur data demonstrates for the first time that portal GLP-1 modulates postprandial and fasting lipids via a complex vagal gut–brain–liver axis. Importantly, loss or interference with this signalling axis via surgical, pharmacological, or dietary intervention resulted in the loss of portal GLP-1s anti-lipemic effects. This supports emerging evidence that native GLP-1 works primarily through a vagal neuroendocrine mechanism.

Effect of Acute Intake of Fermented Orange Juice on Fasting and Postprandial Glucose Metabolism, Plasma Lipids and Antioxidant Status in Healthy Human.

Higher postprandial plasma glucose and lipemia, and oxidative and inflammatory responses, are considered important cardiovascular risk factors. Fermentation of fruits has generated products with high concentrations of bioactive compounds. The aim of this study was to evaluate the potential acute effects that fermented orange juice (FOJ) can exert in healthy humans by modulating postprandial response, and inflammatory/antioxidant status, compared with orange juice (OJ). Nine volunteers were recruited for a randomized, controlled, and crossover study. Participants ingested 500 mL of FOJ. At 4 h post intake, subjects consumed a standardized mixed meal. Blood samples were collected at 0–8 h hours post intake. The subjects repeated the protocol with OJ following a 2-week washout period. Glucose and lipid metabolism, plasma antioxidant capacity (ORAC, FRAP), endogenous antioxidants (albumin, bilirubin, uric acid), C-reactive protein and fibrinogen were measured in plasma samples. There was a trend of a smaller increase in LDL-C after FOJ intake compared with OJ, a significant decrease in apo-B and significant increase in ORAC. The glycemic and triglyceride response of meal was attenuated with FOJ. No differences were obtained in endogenous antioxidants and inflammation status between the treatments. The acute consumption of FOJ could play a protective role against cardiovascular risk factors.

Postprandial Plasma Lipidomics Reveal Specific Alteration of Hepatic-derived Diacylglycerols in Nonalcoholic Fatty Liver Disease

Hepatic energy metabolism is a dynamic process modulated by multiple stimuli. In nonalcoholic fatty liver disease (NAFLD), human studies typically focus on the static fasting state. We hypothesized that unique postprandial alterations in hepatic lipid metabolism are present in NAFLD. In a prospective clinical study, 37 patients with NAFLD and 10 healthy control subjects ingested a standardized liquid meal with pre- and postprandial blood sampling. Postprandial plasma lipid kinetics were characterized at the molecular lipid species level by untargeted lipidomics, cluster analysis, and lipid particle isolation, then confirmed in a mouse model. There was a specific increase of multiple plasma diacylglycerol (DAG) species at 4 hours postprandially in patients with NAFLD but not in controls. This was replicated in a nonalcoholic steatohepatitis mouse model, where postprandial DAGs increased in plasma and concomitantly decreased in the liver. The increase in plasma DAGs appears early in the disease course, is dissociated from NAFLD severity and obesity, and correlates with postprandial insulin levels. Immunocapture isolation of very low density lipoprotein in human samples and stable isotope tracer studies in mice revealed that elevated postprandial plasma DAGs reflect hepatic secretion of endogenous, rather than meal-derived lipids. We identified a selective insulin-related increase in hepatic secretion of endogenously derived DAGs after a mixed meal as a unique feature of NAFLD. DAGs are known to be lipotoxic and associated with atherosclerosis. Although it is still unknown whether the increased exposure to hepatic DAGs contributes to extrahepatic manifestations and cardiovascular risk in NAFLD, our study highlights the importance of extending NAFLD research beyond the fasting state.

Postprandial dyslipidemia after a standardized high-fat meal in BMI-matched healthy individuals, and in subjects with prediabetes or type 2 diabetes

A relationship between postprandial hyperlipidemia and glucose homeostasis/cardiovascular diseases has been suggested. We investigated postprandial plasma lipid patterns after a standardized high-fat meal and their association with glucose homeostasis and subclinical atherosclerosis. Using matching by BMI, 32 healthy individuals with normal glucose tolerance (NGT), 21 subjects with impaired glucose tolerance (IGT), and 20 subjects with drug-naïve type 2 diabetes (T2D) were enrolled. Plasma concentrations of triglycerides (TGs), apolipoprotein-B (ApoB), ApoB48, ApoB100, glucose, and insulin at baseline and 1, 2, 3, 4, 5, 6, and 8h after a standardized meal (1041.03kcal with 70.99g of fat) were measured. Body composition, abdominal visceral fat area, and resting energy expenditure (REE) were measured using dual energy X-ray absorptiometry, computed tomography, and indirect calorimetry, respectively. The intima-media thickness (IMT) of the carotid artery and the ankle-brachial index (ABI) were used to detect subclinical atherosclerosis. Baseline data and area under the curve (AUC) of plasma concentrations of TGs, ApoB, and ApoB48 in the IGT and T2D groups were higher than in the NGT group. The peak TG concentrations after the meal was observed at 5h in subjects with IGT and T2D, while healthy subjects showed the highest concentrations at 4h. In multivariable analysis, high abdominal visceral fat area and low HDL-cholesterol concentrations were independently associated with the AUCTG and AUCApoB after adjusting for confounders including baseline TG and the REE. High LDL-cholesterol and high HbA1c concentrations were also associated with the AUCApoB. Furthermore, high AUCTG and AUCApoB values were independent factors for an increased carotid IMT and a low ABI after adjusting for relevant variables. Abdominal visceral obesity and low HDL-cholesterol concentrations were associated with increased post load excursions of TGs and ApoB in this series. These elevated concentrations of TGs and ApoB were linked with subclinical atherosclerosis.

1215-P: Effects of Exogenous Secretin on Postprandial Plasma Glucose and Lipids and Gallbladder Motility and Hemodynamics in Man

Secretin is best known for its effect on pancreatic exocrine secretion. It also has osmoregulatory effects and was recently identified as a potential target for the treatment of obesity. We investigated the effects of a 5-hour intravenous (iv) secretin infusion on postprandial plasma glucose and lipids and gallbladder motility as well as hemodynamics in healthy males. In a randomized, double-blind, placebo-controlled, crossover study, 25 healthy males (25.7 ± 6.1 (mean ± SD) years; BMI 23.4 ± 1.8 kg/m2) underwent two 5-hour iv infusions of secretin (1 pmol/kg/min) or placebo (saline), with an interposed 8-week washout period. After 30 minutes of infusion, a standardized liquid mixed meal was ingested. Prior to and with regular intervals during the 5-hour infusions, blood samples were drawn, ultrasonography of the gallbladder performed, and hemodynamics measured. Steady-state plasma concentrations of secretin amounted to 113 ± 2 pmol/L, i.e., ~20-fold higher than physiological levels. Postprandial plasma triglyceride excursions were higher during secretin than placebo infusions (baseline-subtracted area under curve: 111 ± 49 vs. 83 ± 36 min × pmol/L [P = 0.012]), whereas excursions in glucose, glycerol and free fatty acids were similar during placebo and secretin infusions. Compared to placebo, secretin reduced maximum gallbladder ejection fraction by 32 ± 27% (P &amp;lt;0.001) and increased mean systolic and diastolic blood pressure by 5.3 ± 4.5 (P &amp;lt;0.039) and 2.2 ± 3.2 mmHg (P &amp;lt;0.001), respectively, and increased heart rate by 5.5 ± 3.6 bpm (P &amp;lt;0.001). We conclude that a 5-hour iv infusion of secretin in healthy males has no effect on fasting and postprandial glucose levels, but reduces postprandial gallbladder contraction, while increasing plasma triglycerides, blood pressure and pulse. Disclosure M. J. Bentzen: None. S. M. Nguyen heimbürger: Speaker’s Bureau; Self; AstraZeneca. B. Hartmann: None. J. J. Holst: Consultant; Self; Novo Nordisk, Other Relationship; Self; Antag Therapeutics, Bainan Biotech, MSD Corporation, Novo Nordisk, Other Relationship; Spouse/Partner; Antag Therapeutics, Bainan Biotech, Synklino ApS. M. B. Christensen: None. F. K. Knop: Advisory Panel; Self; MSD Corporation, Novo Nordisk A/S, Sanofi, Consultant; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Novo Nordisk A/S, Pharmacosmos, Zealand Pharma A/S, Research Support; Self; Novo Nordisk A/S, Zealand Pharma A/S, Speaker’s Bureau; Self; AstraZeneca, Bayer AG, Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, MSD Corporation, Novo Nordisk A/S.

Efficacy of green jackfruit flour as a medical nutrition therapy replacing rice or wheat in patients with type 2 diabetes mellitus: a randomized, double-blind, placebo-controlled study

Background/ObjectivesMedical nutrition therapy along with pharmacological interventions as a multidisciplinary approach is required to treat type 2 diabetes mellitus (T2DM). This study evaluated the efficacy of Jackfruit365™ green jackfruit flour as an integral part of daily meal in patients with T2DM.Subjects/MethodsThis was a randomized, double-blind, placebo-controlled study conducted between May 2019 and February 2020. Patients of either sex aged ≥18 to ≤60 years with a diagnosis of T2DM for >1 year receiving oral antihyperglycemic agents were randomized (1:1) to receive either jackfruit flour 30 g/day (Group A) or placebo flour (Group B) (breakfast and dinner) daily for 12 weeks replacing an equal volume of rice or wheat flour. The primary endpoint was a mean change in glycosylated hemoglobin (HbA1c). Other endpoints were mean changes in fasting plasma glucose (FPG), postprandial plasma glucose (PPG), lipid profile, and body weight. The independent t-test was used to compare changes between the groups.ResultsA total of 40 patients were enrolled (n = 20 each). A significantly higher reduction in HbA1c was observed in Group A compared to Group B from baseline to week 12 [−2.73 mmol/mol (−0.25%) vs. 0.22 mmol/mol (0.02%), p = 0.006]. The mean change in FPG and PPG was significantly higher in Group A than that of Group B (p = 0.043 and p = 0.001). The continuous glucose monitoring showed decreasing mean blood glucose in 7 days of administration of jackfruit flour meal.ConclusionPatients from Group A had a significantly higher reduction in HbA1c, FPG, and PPG than Group B demonstrating the efficacy of jackfruit flour in glycemic control as medical nutrition therapy replacing an equal volume of rice or wheat flour in daily meal.Clinical trial registryCTRI/2019/05/019417.

Comparative effects of insulin glulisine and lispro on postprandial plasma glucose and lipid profile in Japanese patients with type 2 diabetes mellitus

The control of postprandial plasma glucose (PPG) excursions is critical in the prevention of diabetic complications. Controversy remains on the differences in postprandial actions of insulin glulisine and lispro. The aim of this study was to define the differences in the efficacy of these two insulin analogues on PPG. The study subjects were 20 in-hospital patients with type 2 diabetes mellitus (T2DM). Plasma glucose (PG) was tightly controlled with basal insulin and insulin glulisine or lispro, and then glulisine or lispro were switched to the other insulin analog every other day for 6 study days. PG was measured before breakfast and 0.5-, 1-, and 2h-postprandial during the study. Postprandial plasma C-peptide and lipids were analyzed in the first 2days of the study. Postprandial increments in each parameter were compared between glulisine and lispro. Whereas the median value of 0.5h-Δ-PPG was comparable in glulisine and lispro, the 1h-Δ-PPG was significantly lower with lispro than with glulisine (41 vs 53mg/dl, respectively, p = 0.03). Similarly, the 2h-Δ-PPG with lispro was 10mg/dl lower than that with glulisine (35 vs 45mg/dl, respectively, p = 0.05). In parallel with PPG, Δ-C-peptide at 1- and 2h-postprandial were significantly lower with lispro than glulisine (0.50 vs 0.75ng/ml, respectively, and 0.55 vs 0.75ng/ml, respectively). The increment in LDL-C and HDL-C was significantly lower with lispro than with glulisine at 0.5h-postprandial. Insulin lispro seems superior to glulisine in the control of PPG in Japanese patients with T2DM.

Postprandial Apolipoprotein B48 is Associated with Subclinical Atherosclerosis in Patients with Rheumatoid Arthritis.

Objective: To describe postprandial lipemia in patients with rheumatoid arthritis (RA) and to analyze its association with subclinical atherosclerosis measured as carotid intima-media thickness (cIMT). Methods: We performed an observational study of 40 patients with RA and 40 sex and age-matched controls. Patients with dyslipidemia were excluded. Pathologically increased cIMT was defined as a carotid thickness greater than the 90th percentile (>p90) for age and sex. Fasting and postprandial plasma lipids, cholesterol, triglycerides, apolipoprotein B48 (ApoB48), and total ApoB were evaluated. The other variables included were clinical and laboratory values, Framingham score, and the 28-joint Disease Activity Score (DAS28). Two multivariate models were constructed to identify factors associated with pathologic cIMT in patients with RA. Results: Fasting lipid values were similar in patients with RA and controls, although those of postprandial ApoB48 were higher (median (IQR), 14.4 (10.8–12.1) vs. 12.1 (2.3–9,8); p = 0.042). Pathologic cIMT was recorded in 10 patients with RA (25%) and nine controls (22.5%). In patients with RA, pathologic cIMT was associated with postprandial ApoB48 (OR (95% CI), 1.15 (1.0–1.3)) and total ApoB (OR [95% CI], 1.12 [1.1–1.2]). The second model revealed a mean increase of 0.256 mm for cIMT in patients with elevated anticitrullinated protein antibodies (ACPAs). Conclusion: Postprandial ApoB48 levels in patients with RA are higher than in controls. Postprandial ApoB48 and total ApoB levels and markers of severity, such as ACPAs, are associated with pathologic cIMT in patients with RA. Our findings could indicate that these atherogenic particles have a negative effect on the endothelium.

Effect of Atorvastatin on blood ketone levels and glycemic control in patients with type 2 diabetes mellitus: A single arm pilot study

Background and aimsCholesterol and ketone bodies are synthesized in liver from a common precursor acetyl coenzyme A (acetyl-CoA). Statins by inhibiting cholesterol synthesis may lead to accumulation of acetyl-CoA in hepatocytes and its diversion towards ketogenesis. Ketone bodies may act as alternative energy source thus sparing blood glucose and contributing to hyperglycemia. The present study aims to assess the effect of Atorvastatin therapy on blood ketone levels and glycemic control in patients with T2DM. MethodsStudy included 24 statin naïve subjects with T2DM. They were prescribed tablet Atorvastatin at dose of 10 mg once daily at bedtime. Ongoing anti-diabetic medications were not changed. Estimation of blood ketones, urine ketones, fasting plasma glucose (FPG), post-prandial plasma glucose (PPG), glycated hemoglobin (HbA1c) and lipid parameters was carried out at baseline and at 3 months after starting Atorvastatin. ResultsThere was moderate but significant increase in blood ketones (0.16 ± 0.08 mmol/L vs. 0.26 ± 0.07 mmol/L; p-value = 0.0000), FPG (133.8 ± 17.91 mg/dL vs. 143.3 ± 22.99 mg/dL; p-value = 0.0016) and PPG (193.0 ± 36.54 mg/dL vs. 211.0 ± 49.51 mg/dL; p-value = 0.0344) after 3 months of Atorvastatin therapy. This was associated with significant reduction in serum total cholesterol and low density lipoprotein cholesterol. ConclusionThree months therapy with Atorvastatin at the dose of 10 mg once daily at bedtime in patients with T2DM resulted in moderate rise in blood ketone levels, FPG and PPG in addition to improvement in lipid parameters.

Comparative evaluation of biphasic insulin with metformin and triple oral hypoglycemic agents (OHA) in type 2 diabetes patients

IntroductionThe prevalence of secondary failure to oral hypoglycemic agents among type 2 diabetes mellitus (T2DM) patients ranges from 30 to 60%. The alternative approaches to overcome this issue are either switching to triple oral hypoglycemic agents (OHA) or intensifying the regimen by adding insulin. ObjectiveTo compare the glycemic control achieved with biphasic insulin plus metformin and triple OHA in T2DM patients who were not adequately controlled with two OHA regimen. MethodsA qualitative prospective study was conducted at Asir diabetes center, Abha, KSA. Poorly controlled T2DM patients with two OHA for at least 1 year with glycated hemoglobin (HbA1c) >7.0% were included. Subjects were divided into group I (a third OHA was added to the existing two OHA regimen) and group II (switched over to Biphasic insulin and metformin). At baseline and 3-month intervals, level of HbA1C, Fasting Plasma Glucose (FPG), Postprandial Plasma Glucose (PPG), Blood Pressure (BP), lipid profile and hypoglycemic episodes were obtained and evaluated for one year. Results41.1% of patients were in group I and 58.9% were in group II. At the end of the study, there was a significant reduction in HbA1c in group II subjects comparing to group I (8.18 ± 1.32 vs 8.79 ± 1.81, p = 0.0238). FPG and PPG were improved also in group II. The mean body weight increased from baseline in group II is +4.48 kg and decreased from baseline in group I (−0.46 kg). 11.3% from group I and 23.7% from group II reported hypoglycaemic incidences. ConclusionBiphasic insulin and metformin regimen could be an appropriate therapeutic option for achieving good glycemic control compared with triple OHA in patients with two OHA failure.

Shotgun Lipidomics Discovered Diurnal Regulation of Lipid Metabolism Linked to Insulin Sensitivity in Nondiabetic Men.

Meal timing affects metabolic homeostasis and body weight, but how composition and timing of meals affect plasma lipidomics in humans is not well studied. We used high throughput shotgun plasma lipidomics to investigate effects of timing of carbohydrate and fat intake on lipid metabolism and its relation to glycemic control. 29 nondiabetic men consumed (1) a high-carb test meal (MTT-HC) at 09.00 and a high-fat meal (MTT-HF) at 15.40; or (2) MTT-HF at 09.00 and MTT-HC at 15.40. Blood was sampled before and 180 minutes after completion of each MTT. Subcutaneous adipose tissue (SAT) was collected after overnight fast and both MTTs. Prior to each investigation day, participants consumed a 4-week isocaloric diet of the same composition: (1) high-carb meals until 13.30 and high-fat meals between 16.30 and 22:00 or (2) the inverse order. 12 hour daily lipid patterns showed a complex regulation by both the time of day (67.8%) and meal composition (55.4%). A third of lipids showed a diurnal variation in postprandial responses to the same meal with mostly higher responses in the morning than in the afternoon. Triacylglycerols containing shorter and more saturated fatty acids were enriched in the morning. SAT transcripts involved in fatty acid synthesis and desaturation showed no diurnal variation. Diurnal changes of 7 lipid classes were negatively associated with insulin sensitivity, but not with glucose and insulin response or insulin secretion. This study identified postprandial plasma lipid profiles as being strongly affected by meal timing and associated with insulin sensitivity.

Insulin resistance and hyperandrogenemia independently predict nonalcoholic fatty liver disease in women with polycystic ovary syndrome

AimsTo find the prevalence and predictors of nonalcoholic fatty liver disease (NAFLD) in Asian Indian polycystic ovary syndrome (PCOS) women. Materials and methodsThis is a prospective, cross-sectional study conducted at a tertiary care hospital from South India. Sixty women fulfilling the Rotterdam (2003) criteria for PCOS were recruited for the study. All participants were evaluated with ultrasound abdomen for fatty liver and additional biochemical investigations including fasting plasma glucose, postprandial plasma glucose, serum insulin, lipid profile and liver function tests. ResultsThe mean age of the study population was 24.06 ± 5.9 (range: 15–39) years. Oligomenorrhea, hirsutism and acne were present in 58 (96.7%), 37 (61.7%) and 33 (55%) women. Mean BMI of the study population was 29.5 ± 5.28 (range: 19.95 to 45.44) kg/m2. Fifty (83.3%) women were obese (BMI: ≥ 25 kg/m2). Twenty-three (38.3%) women with PCOS had NAFLD. Three women each had isolated elevation of alanine transaminase (ALT) and aspartate transaminases (AST) whereas three women had elevation of both. All women with elevated transaminases had NAFLD. By univariate analysis, factors associated with NAFLD were serum total cholesterol, serum insulin, HOMA-IR, hyperandrogenism, ALT and AST. On multiple regression analysis using linear regression, HOMA-IR and hyperandrogenemia were the only significant predictors of NAFLD. ConclusionOur study reports NAFLD in more than one third of Asian Indian women with PCOS. In addition to insulin resistance (HOMA-IR), hyperandrogenemia is an independent predictor of NAFLD in women with PCOS.

The Role of Visceral Fat, IL-6, Adiponectin and Leptin Levels on Reflux Esophagitis in Obese Patients

Background: Gastroesophageal reflux disease (GERD) is one of the most common problems encountered in clinical practice today. The pathophysiology of GERD is complex, involving diverse factors. Aim of the work: was to assess the role of visceral fat and IL-6, adiponectin and leptin levels on reflux esophagitis in obese patients. Patients and Methods: This prospective observational case-control study included a total of 90 participants; 60 patients with reflux esophagitis and 30 age and sex-matched healthy controls. Evaluation of the Role of Visceral Fat, IL-6, Adiponectin and Leptin Levels on Reflux Esophagitis in Obese Patients was done. Results: An overall 90 patients were enrolled in this study, 50 males and 40 females, were assorted into three groups, obese and had GERD group, non-obese and had GERD, included 30 patients (33.3%),17 males (56.7%) and 13 females (43.3%), and control group, included 30 patients (33.3%),18 males (60%) and 12 females (40%). The mean levels of body mass index, weight circumference, fasting-plasma glaucous, two hours post-prandial plasma glucose, Creatinine, liver enzymes, and lipid parameters were elevated in obese group when compared with non-obese and control groups. Consequently, the mean levels of leptin and interleukin-6 were high in obese group in comparison with other groups. Interestingly, the mean level of adiponectin was high in non-obese group in comparison with obese and control groups. Conclusion: Inflammatory cytokines, adipokines, and visceral fat referring abdominal obesity had an association with reflux esophagitis.

The Role of Visceral Fat, IL-6, Adiponectin and Leptin Levels on Reflux Esophagitis in Obese Patients

Background: Gastroesophageal reflux disease (GERD) is one of the most common problems encountered in clinical practice today. The pathophysiology of GERD is complex, involving diverse factors. Aim of the work: was to assess the role of visceral fat and IL-6, adiponectin and leptin levels on reflux esophagitis in obese patients. Patients and Methods: This prospective observational case-control study included a total of 90 participants; 60 patients with reflux esophagitis and 30 age and sex-matched healthy controls. Evaluation of the Role of Visceral Fat, IL-6, Adiponectin and Leptin Levels on Reflux Esophagitis in Obese Patients was done. Results: An overall 90 patients were enrolled in this study, 50 males and 40 females, were assorted into three groups, obese and had GERD group, non-obese and had GERD, included 30 patients (33.3%),17 males (56.7%) and 13 females (43.3%), and control group, included 30 patients (33.3%),18 males (60%) and 12 females (40%). The mean levels of body mass index, weight circumference, fasting-plasma glaucous, two hours post-prandial plasma glucose, Creatinine, liver enzymes, and lipid parameters were elevated in obese group when compared with non-obese and control groups. Consequently, the mean levels of leptin and interleukin-6 were high in obese group in comparison with other groups. Interestingly, the mean level of adiponectin was high in non-obese group in comparison with obese and control groups. Conclusion: Inflammatory cytokines, adipokines, and visceral fat referring abdominal obesity had an association with reflux esophagitis.

A 12-wk whole-grain wheat intervention protects against hepatic fat: the Graandioos study, a randomized trial in overweight subjects

Whole-grain wheat (WGW) is described as nutritionally superior to refined wheat (RW) and thus advocated as the healthy choice, although evidence from intervention studies is often inconsistent. The liver, as the central organ in energy metabolism, might be an important target organ for WGW interventions. The aim of this study was to investigate the potential benefits of WGW consumption compared with RW consumption on liver health and associated parameters. We performed a double-blind, parallel trial in which 50 overweight 45- to 70-y-old men and postmenopausal women were randomly allocated to a 12-wk intervention with either WGW (98 g/d) or RW (98 g/d) products. Before and after the intervention we assessed intrahepatic triglycerides (IHTGs) and fat distribution by proton magnetic resonance spectroscopy/magnetic resonance imaging, fecal microbiota composition, adipose tissue gene expression, and several fasting plasma parameters, as well as postprandial plasma lipids after a mixed meal. Fasting plasma cholesterol, triglycerides, nonesterified fatty acids, and insulin were not affected by RW or WGW intervention. We observed a substantial increase of 49.1% in IHTGs in the RW when compared with the WGW group (P=0.033). Baseline microbiota composition could not predict the increase in IHTGs after RW, but gut microbiota diversity decreased in the RW group when compared with the WGW group (P=0.010). In the WGW group, we observed increased postprandial triglyceride levels compared with the RW group (P=0.020). In addition, the WGW intervention resulted in a trend towards lower fasting levels of the liver acute-phase proteins serum amyloid A (P=0.057) and C-reactive protein (P=0.064) when compared to the RW intervention. A 12-wk RW intervention increases liver fat and might contribute to the development of nonalcoholic fatty liver disease, whereas a 12-wk 98-g/d WGW intervention prevents a substantial increase in liver fat. Our results show that incorporating feasible doses of WGW in the diet at the expense of RW maintains liver health. The study was registered at clinicaltrials.gov as NCT02385149.

Association of Vitamin D Levels and type 2 Diabetes Mellitus in Asian Indians is Independent of Obesity.

A large proportion of subjects with type 2 diabetes mellitus (T2DM) in India are non-obese. Asian-Indian subjects with diabetes have been shown to have low vitamin D levels. Whether low vitamin D levels and T2DM in Asian-Indians is attributable to the associated obesity as in caucasians is unclear. Hence we studied the association of vitamin D levels and T2DM in Asian-Indians with or without obesity. Total of 213 subjects were recruited in four groups, group 1-Non-obese diabetic, group 2-Non-obese non-diabetic, group 3-Obese diabetic and group 4-Obese non-diabetic. Subjects recruited under various groups were matched for age and sex. Anthropometry, skin-fold thickness, fasting and postprandial plasma glucose, HbA1c, fasting insulin, lipids and vitamin D levels were measured in all study subjects and were compared between the groups. Mean age of study population was 41.23±7.43 years. Mean BMI in groups 1,2,3 and 4 was 21.34±1.41, 20.53±2.27, 27.72±2.94 and 27.62±3.37 kg/m2 respectively. Overall 64.3% study subjects had vitamin D deficiency and 27.7% had insufficient vitamin D levels. Significantly lower vitamin D levels were found in diabetic groups 1 and 3 compared to non-diabetic groups 2 and 4. No significant difference was observed in vitamin D levels between groups 1 and 3. Similarly, no significant difference was observed in vitamin D levels between groups 2 and 4. Vitamin D levels did not show any significant correlation with BMI, waist or body fat. Vitamin D levels do not appear to be related to obesity in diabetic as well non-diabetic Asian-Indian individuals.

Acute effect of Clitoria ternatea flower beverage on glycemic response and antioxidant capacity in healthy subjects: a randomized crossover trial

BackgroundClitoria ternatea L., a natural food-colorant containing anthocyanin, demonstrated antioxidant and antihyperglycemic activity. The aim of this study was to determine the effects of Clitoria ternatea flower extract (CTE) on postprandial plasma glycemia response and antioxidant status in healthy men.MethodsIn a randomized, crossover study, 15 healthy men (ages 22.53 ± 0.30 years; with body mass index of 21.57 ± 0.54 kg/m2) consumed five beverages: (1) 50 g sucrose in 400 mL water; (2) 1 g CTE in 400 mL of water; (3) 2 g CTE in 400 mL of water; (4) 50 g sucrose and 1 g CTE in 400 mL of water; and (5) 50 g sucrose and 2 g CTE in 400 mL of water. Incremental postprandial plasma glucose, insulin, uric acid, antioxidant capacities and lipid peroxidation were measured during 3 h of administration.ResultsAfter 30 min ingestion, the postprandial plasma glucose and insulin levels were suppressed when consuming sucrose plus 1 g and 2 g CTE. In addition, consumption of CTE alone did not alter plasma glucose and insulin concentration in the fasting state. The significant increase in plasma antioxidant capacity (ferric reducing ability of plasma (FRAP), oxygen radical absorbance capacity (ORAC), trolox equivalent antioxidant capacity (TEAC), and protein thiol) and the decrease in malondialdehyde (MDA) level were observed in the subjects who received 1 g and 2 g CTE. Furthermore, consumption of CTE protected sucrose-induced reduction in ORAC and TEAC and increase in plasma MDA.ConclusionsThese findings suggest that an acute ingestion of CTE increases plasma antioxidant capacity without hypoglycemia in the fasting state. It also improves postprandial glucose, insulin and antioxidant status when consumed with sucrose.Trial registrationThai Clinical Trials Registry: TCTR20170609003. Registered 09 September 2017.‘retrospectively registered’.

Abstract 601: Global and Liver Specific Bmal1 Deficient Mice Regulate Intestinal Lipid Absorption

Circadian rhythms controlled by clock genes affect plasma lipids, known risk factors for atherosclerosis. Clock and Bmal1 are critical clock genes that positively regulate circadian rhythms. We have shown that Clock plays an important role in lipid absorption. Additionally, we showed that global ablation of Bmal1 in Apoe –/– and Ldlr –/– mice, and liver-specific ablation of Bmal1 in Apoe –/– (L -Bmal1 –/– Apoe –/– ) mice increases atherosclerosis. However, it is unknown whether Bmal1 regulates intestinal lipid absorption. We studied cholesterol and triglyceride absorption in normal and lipase-inhibited Bmal1 –/– and Bmal1 –/– Apoe –/– mice with global Bmal1 deficiency and compared it with Bmal1 +/+ and Bmal1 +/+ Apoe –/– , respectively. To study the effect of liver-specific Bmal1 deficiency, studies were performed in L- Bmal1 –/– and L- Bmal1 –/– Apoe –/– mice and data were compared with Bmal1 fl/fl and Bmal1 fl/fl Apoe –/– mice. In addition, enterocytes isolated from these mice were used to study uptake and secretion of cholesterol and oleic acid. Further, protein and mRNA levels of candidate genes involved in lipid uptake, lipoprotein assembly and secretion were quantified. Both normal and lipase-inhibited Bmal1 –/– mice absorbed significantly higher amounts of cholesterol and triglyceride. Further, uptake and secretion of cholesterol and fatty acids by enterocytes was increased in Bmal1 –/– mice. As reported previously, liver-specific Bmal1 ablation increased VLDL production. Surprisingly, postprandial plasma lipids were also significantly increased in L- Bmal1 –/– mice than in control Bmal1 fl/fl mice. Further, enterocytes isolated from L- Bmal1 –/– took up more lipids and secreted more lipoproteins. Moreover, in vivo lipid absorption in L- Bmal1 –/– was increased. Gene expression quantifications revealed that intestinal MTP, DGAT1, CD36 and NPC1L1 mRNA levels were increased in global and hepatic Bmal1 deficient animals. Global and liver-specific ablation of Bmal1 increases intestinal lipoprotein production by increasing the expression of genes involved in lipid uptake and lipoprotein assembly. These data for the first time suggest that intestinal lipoprotein assembly is regulated by hepatic Bmal1.