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Oxidative Stress and the Effects of Dietary Supplements on Glycemic Control in Type 2 Diabetes
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
A recent study has examined the effect of vitamin E supplementation on glycemic control in type 2 diabetic patients on metformin treatment. In this study, 40 type 2 diabetic male patients aged 40–60 years on metformin (500 mg twice daily) treatment were randomly divided into four groups, with each group receiving an additional one of the following twice-daily oral supplements for 90days: placebo, vitamin C (500 mg), vitamin E (400 mg), and vitamin C (500 mg) plus vitamin E (400 mg). As shown in Table 23.1, it was found that, in the patients receiving vitamin C and/or vitamin E, fasting blood sugar, hemoglobin A1c (HbA1c), lipid profile, insulin, and homeostasis model assessment-insulin resistance (HOMA-IR), GSH and quantitative insulin sensitivity check index (QISCI) improved significantly when compared to the control group receiving placebo [61]. This study thus provides strong support for the use of vitamin E or vitamin C as adjuvant therapy in the management of patients with type 2 diabetes.
Selected Functional Foods That Combat the Effects of Hyperglycemia and Chronic Inflammation
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Similarly, a clinical study with conventional protocols, published in the International Journal of Food Science and Nutrition, reported that ginger supplementation significantly lowered the levels of insulin (11.0 ± 2.3 vs. 12.1 ± 3.3), LDL cholesterol (67.8 ± 27.2 vs. 89.2 ± 24.9), TG (127.7 ± 43.7 vs. 128.2 ± 37.7), and the HOMA index (3.9 ± 1.09 vs. 4.5 ± 1.8), and increased the QUICKI (0.313 ± 0.012 vs. 0.308 ± 0.012) in comparison to a control group. The quantitative insulin sensitivity check index (QUICKI) is determined by the inverse of the sum of the logarithms of the fasting insulin and fasting glucose: 1/(log(fasting insulin μU/mL) + log(fasting glucose mg/dL)).
The drug dilemma of oral antidiabetic agents in pregnancy: Metformin
Published in Moshe Hod, Lois G. Jovanovic, Gian Carlo Di Renzo, Alberto de Leiva, Oded Langer, Textbook of Diabetes and Pregnancy, 2018
Yoel Toledano, Moshe Zloczower, Nicky Lieberman
However, there is currently no validated test for measuring insulin resistance in a clinical setting. Serum triglyceride concentration, the ratio of triglyceride to high-density lipoprotein (HDL)-cholesterol concentrations, and fasting insulin concentration are useful markers for identifying those who may be insulin resistant.34 Optimal cut-points were identified as 130 mg/dL (1.47 mmol/L), 3.0 (1.8 SI units), and 109 pmol/L for triglycerides, triglyceride-to-HDL ratio, and insulin, respectively.35 Sensitivity and specificity for the cut-points were 67%, 64%, and 57%, and 71%, 68%, and 85%, respectively. In large population epidemiology studies, simple ratios derived from fasting insulin and glucose (e.g., glucose to insulin ratios, homeostasis model assessment of insulin resistance [HOMA-IR or HOMA]) have been extensively used. There are limitations to their use, including changes in beta cell function over time, lack of a standardized universal insulin assay, and lack of data demonstrating that markers of insulin resistance predict response to treatment. As a result, although indexes such as HOMA and QUICKI (quantitative insulin sensitivity check index) have been proposed and cut-points identified,36 none are recommended for routine assessment of insulin resistance in the clinic.
Urine sodium excretion is related to extracellular water volume but not to blood pressure in 510 normotensive and never-treated hypertensive subjects
Published in Blood Pressure, 2023
Jyrki Taurio, Jenni Koskela, Marjatta Sinisalo, Antti Tikkakoski, Onni Niemelä, Mari Hämäläinen, Eeva Moilanen, Manoj Kumar Choudhary, Jukka Mustonen, Pasi Nevalainen, Ilkka Pörsti
The participants collected 24-h urine, and blood and urine samples were taken after about 12 h of fasting. Plasma and urine electrolytes, and plasma cystatin C, creatinine, C-reactive protein (CRP), glucose, uric acid and lipid determinations were performed using Cobas Integra 700/800 (F. Hoffmann-LaRoche Ltd., Basel, Switzerland) or Cobas 6000, module c501 (Roche Diagnostics, Basel, Switzerland). Plasma calcidiol (25(OH)D3) and calcitriol (1,25(OH)2D3) were analysed using enzyme immunoassay (Immunodiagnostic Systems, Boldon, UK) and parathyroid hormone (PTH) and insulin using electrochemiluminescence immunoassay (Cobas e411, Roche Diagnostics). Quantitative insulin sensitivity check index (QUICKI) was calculated from fasting plasma insulin and glucose [21]. Blood cell counts were analysed using ADVIA 120 or 2120 (Bayer Health Care, Tarrytown, NY, USA). Kidney disease exclusion was by estimated GFR (CKD-EPI cystatin C formula [22]) and by refractometric dipstick analysis and nephelometric analysis of urine albumin (Clinitec Atlas or Advantus and BN Prospec, respectively, Siemens Healthcare GmbH, Erlangen, Germany).
Inflammatory Potential of Diet: Association With Chemerin, Omentin, Lipopolysaccharide-Binding Protein, and Insulin Resistance in the Apparently Healthy Obese
Published in Journal of the American College of Nutrition, 2019
Susan Mirmajidi, Azimeh Izadi, Maryam Saghafi-Asl, Farhad Vahid, Nahid Karamzad, Parichehr Amiri, Nitin Shivappa, James R. Hébert
After an overnight fast, blood samples were drawn and serum was separated by centrifuging at 3000 rpm for 15 min. Lipid profile and blood sugar were measured immediately, using a commercial kit (Pars Azmoon, Tehran, Iran) and a Selectra 2 autoanalyzer (Vital Scientific, Spankeren, the Netherlands). Interassay and intra-assay coefficients of variation (CV) were <5% for all assays). The rest of the serum samples were stored at −80ºC until analysis. Serum insulin, LBP, chemerin, and omentin levels were determined by a sandwich enzyme-linked immunosorbent assay (ELISA), using commercial kits (insulin: Monobind, Inc., lake Forest, CA; and other parameters: Bioassay Technology Laboratory, Shanghai Korean Biotech, Shanghai City, China), according to the manufacturer’s instructions. The intra-assay and interassay CVs were <8% and 10% for chemerin, omentin, and LBP and <8% and 9.8% for insulin, respectively. The homeostasis model assessment of IR (HOMA-IR) was calculated, using fasting plasma glucose and fasting insulin values, according to the formula (37). Quantitative insulin sensitivity check index (QUICKI) was calculated based on the formula, with higher QUICKI values, indicating greater insulin sensitivity. The homeostasis model assessment of beta cells (HOMA-B) was also used to estimate pancreatic beta cell function (38).
The effect of vitamin D supplementation on insulin resistance, visceral fat and adiponectin in vitamin D deficient women with polycystic ovary syndrome: a randomized placebo-controlled trial
Published in Gynecological Endocrinology, 2018
Maryam Seyyed Abootorabi, Parvin Ayremlou, Tahereh Behroozi-Lak, Sakineh Nourisaeidlou
Twelve-hour fasting blood samples were collected at baseline and week 8 of the intervention. The Blood samples were immediately centrifuged at 4000 rpm for 10 min to separate serum and the serum was stored at −70 °C until assayed. All tests were conducted at reference laboratory of Urmia Shahid Motahhari Hospital and by a person. The serum was used for determination of fasting plasma glucose (FBS), insulin, 25 (OH) D levels, and adiponectin. Serum 25-hydroxyvitamin D concentrations were assessed using a commercial ELISA kit (Roche, UK). Fasting plasma glucose was measured by enzymatic colorimetric method using glucose oxidase kit (Pars Azmoon Inc., Tehran, Iran). Serum insulin was assayed by ELISA kit (monobind, Lake Forest, CA). Insulin resistance was measured using the HOMA-IR method ([fasting insulin {[fasting insulin (μU/mL)] × [fasting glucose (mmol/L)]/22.5 (RA). Insulin sensitivity was measured using the quantitative insulin sensitivity check index (QUICKI; 1/[log (fasting insulin, μU/mL) + log (fasting glucose, mg/dL)] [25]. sensitivity estimated by homeostasis model assessment of beta cell function (HOMA-B [20 × fasting insulin (μU/mL)]/[fasting glucose (mmol/L) – 3/5] [1]. Adiponectin was assayed by ELISA kit (zellbio, UK).