scholarly journals Prevalence of Vitamin D Deficiency and Its Association with Insulin Resistance in Obese Women with Normal Fasting Glucose

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Nazish Saleem ◽  
Nayab Batool Rizvi ◽  
Shan Elahi
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Fasting Glucose ◽  
Univariate Analysis ◽  
Multivariate Regression Analysis ◽  
Fasting Insulin ◽  
Obese Women ◽  
Insulin Resistant ◽  
Serum Pth

Background and Objective. Association of vitamin D (25-hydroxyvitamin-D; 25(OH)D), with glucose metabolism is ethnic dependent. We study the relation of vitamin D and its metabolites with the glycemic profile of obese women. Patients and Methods. Informed consent and demographic information was collected from obese ( BMI ≥ 30   kg / m 2 ) and nonobese women. A blood sample in fasting was obtained and analyzed for fasting glucose, fasting insulin, serum 25(OH)D, serum parathyroid hormone (PTH), and calcium levels. Insulin resistance (IR), detected by Matthews’ method (1985), was considered in women with HOMA − IR ≥ 2.5 . Vitamin   D   concentrations < 12   ng / ml were considered vitamin D deficiency. Results. A total of 264 obese and 133 normal BMI women (controls) of age range 20-50 years were selected. Obese women had significantly lower vitamin D compared to control women ( P < 0.05 ). Among euglycemic ( fasting   glucose < 100   mg / dl ) obese women ( n = 221 ), 90 (40.7%) were vitamin D deficient. Serum PTH and calcium levels were negatively correlated, though nonsignificantly with vitamin D ( r = − 0.172 , P = 0.090 , and r = − 0.051 , P = 0.557 , respectively). The mean age, BMI, waist circumference (WC), hip circumference (HC), waist-to-hip ratio (WHR), fasting glucose, fasting insulin, PTH, and calcium were not significantly different in vitamin D-deficient as compared to nondeficient obese women. IR was detected in 109 (49.3%) obese women. Mean HOMA-IR in vitamin D-deficient women was significantly higher than that in the nondeficient obese women ( 3.03 ± 1.64 vs. 2.40 ± 1.02 ; P = 0.041 ), but the percentage of women with IR was comparable in both groups (51.1% vs. 45.8%; P = 0.745 ). Univariate analysis revealed that HOMA-IR was negatively correlated with vitamin D and positively with BMI and PTH. A multivariate regression analysis, stepwise method revealed that BMI and PTH were independent determinants of HOMA-IR instead of vitamin D. Conclusion. More than 40% of obese women were vitamin D deficient. Among euglycemic obese women, 49% were insulin resistant. Prevalence of insulin resistance, though negatively correlated with vitamin D, could be better explained by BMI and PTH levels.

The Relationship Between Vitamin D Deficiency and Insulin Resistance in Pregnant Women with Gestational Diabetes

2019 ◽  
Vol 15 (5) ◽  
pp. 414-419 ◽  
Author(s):  
Zahra Mazloum Khorasani ◽  
Shokoufeh Bonakdaran ◽  
Hasan Pour Rafieie
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Vitamin D ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Vitamin D Deficiency ◽  
P Value ◽  
Insulin Resistant ◽  
Medical Disorders ◽  
Resistant Group

Background: Diabetes Mellitus is one of the most common medical disorders in pregnancy. The possibility of vitamin D deficiency as a pathogenesis for impaired glucose tolerance tests show a probable role of vitamin D in insulin secretion and reduction of insulin resistance. This study was assigned to evaluate relation between serum vitamin D level and insulin resistance in Gestational Diabetes Mellitus (GDM). Methods: This cross sectional study was done throughout one year between 2015-2016 in GDM patients (age, 20-40 years). After history taking and physical examination, the laboratory tests including : Fasting Blood Sugar (FBS), Glucose Tolerance Test (GTT), calcium, phosphorous, parathormone, 25(OH) vitamin D, insulin, HbA1C, TG, LDL, HDL were performed for all patients. Insulin resistance was calculated according to HOMA-IR formula. Vitamin D level was compared between patients with and without insulin resistance. Results: This research was performed in 93 GDM patients with average age (30.3 ± 5.6). Thirty eight patients with insulin resistance and 55 patients without insulin resistance were detected. The prevalence of vitamin D deficiency was 91.4% in all patients. There was no significant difference in vitamin D levels between insulin resistant and non insulin resistant group (P-value=0.51). : In all variable parameters, only FBS and triglyceride level in insulin resistant group were more than non insulin resistant group (P-value<0.05). : Obtained results showed not significant relationship between vitamin D deficiency and insulin resistance in GDM patients.

Waist circumference and cardiorespiratory fitness are independently associated with glucose tolerance and insulin resistance in obese women

2014 ◽  
Vol 39 (3) ◽  
pp. 358-362 ◽  
Author(s):  
Einat Shalev-Goldman ◽  
K. Ashlee McGuire ◽  
Robert Ross
Keyword(s):  
Insulin Resistance ◽  
Waist Circumference ◽  
Glucose Tolerance ◽  
Cardiorespiratory Fitness ◽  
Fasting Glucose ◽  
Tolerance Test ◽  
Fasting Insulin ◽  
Obese Women ◽  
Insulin Metabolism ◽  
The Relationship

The purpose of this study was to determine the independent associations between physical activity (PA), cardiorespiratory fitness (CRF), abdominal obesity and insulin action in obese women. We studied 141 abdominally obese women (waist circumference (WC): 106.4 ± 10.2 cm). PA duration (min/day) and intensity (counts/min) were obtained by accelerometry. CRF was measured using a treadmill. WC was measured at the iliac crest; abdominal adiposity was measured by magnetic resonance imaging. Glucose and insulin measures were obtained during a 75-g, 2-h glucose tolerance test. The homeostasis model of assessment iHOMA2-IS was used to estimate insulin sensitivity. PA duration and intensity were not associated with glucose or insulin metabolism (p > 0.05). However, moderate-to-vigorous PA (MVPA) duration was associated with fasting insulin and iHOMA2-IS (p < 0.01). CRF was associated with fasting insulin and iHOMA2-IS (r = 0.27, p ≤ 0.01), whereas WC was associated with fasting insulin (r = 0.50, p < 0.01) and iHOMA2-IS (r = –0.52, p ≤ 0.01). Following adjustment for CRF, MVPA, and age, WC remained associated with fasting glucose, insulin, 2-h glucose and iHOMA2-IS (r = –0.44, p ≤ 0.01). CRF was associated with fasting glucose as well as 1- and 2-h glucose (r = 0.24, p < 0.01) after adjusting for WC, MVPA, and age. MVPA was not associated with glucose or insulin measures after control for CRF and WC (p > 0.05). Mediation analysis revealed that CRF and WC combined mediated the relationship between MVPA and both glucose tolerance and insulin resistance (p < 0.05). In conclusion, among abdominally obese women, WC and CRF are independently associated with measures of glucose tolerance and insulin resistance and mediate the association between MVPA and insulin resistance.

scholarly journals Insulin sensitizing drugs increase the endogenous dopaminergic tone in obese insulin-resistant women with polycystic ovary syndrome

2005 ◽  
Vol 184 (1) ◽  
pp. 233-239 ◽  
Author(s):  
C Ortega-González ◽  
L Cardoza ◽  
B Coutiño ◽  
R Hidalgo ◽  
G Arteaga-Troncoso ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Polycystic Ovary Syndrome ◽  
Fasting Glucose ◽  
Polycystic Ovary ◽  
Serum Insulin ◽  
Oral Glucose ◽  
Obese Women ◽  
Ovary Syndrome ◽  
Insulin Resistant

To investigate whether the long-term administration of metformin or pioglitazone to women with polycystic ovary syndrome (PCOS) could induce changes in their hypothalamic dopaminergic (DA) tone and to analyze whether these changes correlated with modifications in insulin resistance, we originally studied 57 obese hyperinsulinemic, non-diabetic, insulin resistant women with PCOS, but only 34 completed the study. They were randomly divided into two groups: group one (n=17) received pioglitazone (30 mg/day) and group 2 (n=17) received metformin (850 mg, three times a day) over 24 weeks. All women were identically studied before (basal) and 6 months after (T6) drug administration, including clinical evaluations, a 2 h oral glucose tolerance test (75 g) (OGTT) for glucose and insulin measurements, followed a week later by a 2 h intravenous metoclopramide test (10 mg bolus) for prolactin (PRL) determinations. The areas under the insulin (AUC-insulin) and PRL (AUC-PRL) curves were calculated, along with the index of insulin resistance (HOMA-IR) and the indexes of insulin sensitivity (QUICKI and fasting glucose–insulin ratio). At baseline, women in both groups were of similar age, body weight, body mass index (BMI) and Ferriman-Gallwey hirsutism score (F-G score). At completion of the study, body weight and BMI remained unchanged but the F-G score significantly decreased. Fasting serum insulin concentrations and the AUC-insulin significantly decreased by the end of the trial in a similar fashion in both groups, while the AUC-PRL significantly increased at the end of the trial in both groups. At no time were significant correlations between AUC-PRL and AUC-insulin or the indexes HOMA-IR, QUICKI or fasting glucose–insulin ratio observed. The present results suggests that either pioglitazone or metformin administration was associated with a clear improvement in the endogenous hypothalamic DA tone, simultaneously with an amelioration of the insulin resistance status in these obese women with PCOS.

scholarly journals Is Vitamin D Deficiency Related to Increased Cancer Risk in Patients with Type 2 Diabetes Mellitus?

2021 ◽  
Vol 22 (12) ◽  
pp. 6444
Author(s):  
Anna Gabryanczyk ◽  
Sylwia Klimczak ◽  
Izabela Szymczak-Pajor ◽  
Agnieszka Śliwińska
Keyword(s):  
Diabetes Mellitus ◽  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Vitamin D ◽  
Cancer Risk ◽  
Vitamin D Deficiency ◽  
Cancer Development ◽  
Increased Risk

There is mounting evidence that type 2 diabetes mellitus (T2DM) is related with increased risk for the development of cancer. Apart from shared common risk factors typical for both diseases, diabetes driven factors including hyperinsulinemia, insulin resistance, hyperglycemia and low grade chronic inflammation are of great importance. Recently, vitamin D deficiency was reported to be associated with the pathogenesis of numerous diseases, including T2DM and cancer. However, little is known whether vitamin D deficiency may be responsible for elevated cancer risk development in T2DM patients. Therefore, the aim of the current review is to identify the molecular mechanisms by which vitamin D deficiency may contribute to cancer development in T2DM patients. Vitamin D via alleviation of insulin resistance, hyperglycemia, oxidative stress and inflammation reduces diabetes driven cancer risk factors. Moreover, vitamin D strengthens the DNA repair process, and regulates apoptosis and autophagy of cancer cells as well as signaling pathways involved in tumorigenesis i.e., tumor growth factor β (TGFβ), insulin-like growth factor (IGF) and Wnt-β-Cathenin. It should also be underlined that many types of cancer cells present alterations in vitamin D metabolism and action as a result of Vitamin D Receptor (VDR) and CYP27B1 expression dysregulation. Although, numerous studies revealed that adequate vitamin D concentration prevents or delays T2DM and cancer development, little is known how the vitamin affects cancer risk among T2DM patients. There is a pressing need for randomized clinical trials to clarify whether vitamin D deficiency may be a factor responsible for increased risk of cancer in T2DM patients, and whether the use of the vitamin by patients with diabetes and cancer may improve cancer prognosis and metabolic control of diabetes.

scholarly journals Pharyngeal collapsibility during sleep is elevated in insulin-resistant females with morbid obesity

2016 ◽  
Vol 47 (6) ◽  
pp. 1718-1726 ◽  
Author(s):  
Oscar L. Llanos ◽  
Panagis Galiatsatos ◽  
Edmarie Guzmán-Vélez ◽  
Susheel P. Patil ◽  
Philip L. Smith ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fasting Glucose ◽  
Sleep Apnoea ◽  
Model Assessment ◽  
Rapid Eye Movement Sleep ◽  
Homeostasis Model Assessment ◽  
Tonsillar Hypertrophy ◽  
Insulin Resistant ◽  
Bariatric Patients ◽  
Respiratory Disturbance

Insulin resistance is associated with sleep apnoea, leading us to hypothesise that it is also associated with elevations in pharyngeal collapsibility, even in the absence of sleep apnoea.90 bariatric patients were characterised for sleep apnoea, pharyngeal collapsibility and insulin resistance. Patients with a respiratory disturbance index (RDI) >10 events·h−1, diabetes mellitus, tonsillar hypertrophy and pulmonary disease were excluded. The remaining 14 females underwent collapsibility measurements (passive critical pressure, Pcritp) during non-rapid eye movement sleep. The homeostasis model assessment (HOMA) index, a measure of insulin resistance, was derived from measurements of fasting glucose and insulin levels, and compared to Pcritp.Groups with high Pcritp compared to low Pcritp did not differ in age, body mass index or RDI. HOMA and insulin were elevated in the high Pcritp group compared to the low Pcritp group (p<0.02). Pcritp correlated with HOMA (Spearman's ρ=0.565, 95% CI 0.104–0.862; p=0.035) and insulin (Spearman's ρ=0.609 95% CI 0.196–0.835; p=0.021).Obese insulin-resistant subjects without frank diabetes or sleep apnoea demonstrate preclinical elevations in pharyngeal collapsibility, which may increase their susceptibility to sleep apnoea. Our findings suggest that insulin resistance could play a significant role in sleep apnoea pathogenesis by generating requisite elevations in pharyngeal collapsibility.

scholarly journals The Decreased Growth Hormone Response to Growth Hormone Releasing Hormone in Obesity Is Associated to Cardiometabolic Risk Factors

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Fernando Cordido ◽  
Jesús Garcia-Buela ◽  
Susana Sangiao-Alvarellos ◽  
Teresa Martinez ◽  
Ovidio Vidal
Keyword(s):  
Insulin Resistance ◽  
Growth Hormone ◽  
Cardiovascular Risk ◽  
Ldl Cholesterol ◽  
Premenopausal Women ◽  
Fasting Insulin ◽  
Risk Markers ◽  
Obese Women ◽  
Gh Secretion ◽  
The Metabolic Syndrome

The aim of the present study was to evaluate the relationship between GHRH-induced GH secretion in obese premenopausal women and cardiovascular risk markers or insulin resistance. Premenopausal obese women, aged 35–52 years, were studied. GH secretion, IGF-I, serum cardiovascular risk markers, insulin, leptin, mid-waist and hip circumference, total body fat, and truncal fat were measured. Subjects were classified as meeting the criteria for GH deficiency (GHD) when peak GH after stimulation with GHRH was≤3 μg/L. Mean total and LDL cholesterol, fasting insulin, and HOMA-IR were all higher, in subjects who would have been classified as GH-deficient compared with GH-sufficient. Peak GH secretion after stimulation was inversely associated with fasting insulin (R=−0.650,P=.012), HOMA-IR (R=−0.846,P=.001), total cholesterol (R=−0.532,P=.034), and LDL cholesterol (R=−0.692,P=.006) and positively associated with HDL cholesterol (R=0.561,P=.037). These data strongly suggest a role for insulin resistance in the decreased GH secretion of obesity and that the blunted GH secretion of central obesity could be the pituitary expression of the metabolic syndrome.

scholarly journals Kefir reduces insulin resistance and inflammatory cytokine expression in an animal model of metabolic syndrome

2016 ◽  
Vol 7 (8) ◽  
pp. 3390-3401 ◽  
Author(s):  
Damiana D. Rosa ◽  
Łukasz M. Grześkowiak ◽  
Célia L. L. F. Ferreira ◽  
Ana Carolina M. Fonseca ◽  
Sandra A. Reis ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Animal Model ◽  
Inflammatory Cytokine ◽  
Fasting Glucose ◽  
Cytokine Expression ◽  
Fasting Insulin ◽  
Insulin Levels ◽  
Reduce Insulin Resistance

Kefir supplementation in rats with induced metabolic syndrome was able to lower fasting glucose, fasting insulin levels, and reduce insulin resistance.

Sex Dependent Association of Vitamin D with Insulin Resistance

2021 ◽  
Author(s):  
Xin Chen ◽  
Chang Chu ◽  
Cornelia Doebis ◽  
Volker von Baehr ◽  
Berthold Hocher
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Animal Studies ◽  
Linear Regression Analysis ◽  
Cross Sectional Study ◽  
Multivariate Linear Regression Analysis ◽  
Double Blind ◽  
Cross Sectional ◽  
Entire Study

Abstract Background Animal studies suggested that vitamin D might decrease insulin resistance. Estrogen increased insulin sensitivity and glucose tolerance in rodents. However, sex-specific association of vitamin D with insulin resistance in humans remains unclear. Objectives To investigate the sex-dependency of the association of insulin resistance and 25(OH)D in a large Caucasian population. Methods Cross-sectional study from out-patients’ blood samples with measurements of 25(OH)D and HOMA-IR drawn at exactly the same day (N=1887). This cohort was divided into three groups: i) group with vitamin D deficiency (n=1190), ii) group with vitamin D sufficiency (N=686)), iii) vitamin D excess groups (n=11), the vitamin D excess group was excluded from further analysis due to the small size. Results Analysis of the entire study population showed that serum 25-hydroxyvitamin D was inversely associated with HOMA-IR (rs=-0.19, P&lt;0.0001). When considering the vitamin D status, this association was only seen in the vitamin D deficiency group, but not in the vitamin D sufficient group. The correlation was sex-dependent: HOMA-IR was inversely correlated with vitamin D in women with vitamin D deficiency (rs=-0.26, P&lt;0.0001) but not in men with vitamin D deficiency (rs=0.01, P=0.714). After multivariate linear regression analysis considering confounding factors, this relationship was again only seen in women. Conclusion Vitamin D was inversely and independently associated with insulin resistance only in women with vitamin D deficiency. Based on our data, we suggest that in particular vitamin D deficient women might benefit from vitamin D substitution by improving insulin resistance. This, however, needs to be proven in adequately designed double-blind placebo-controlled clinical studies.

GLP-1 response to sequential mixed meals: influence of insulin resistance

2017 ◽  
Vol 131 (24) ◽  
pp. 2901-2910 ◽  
Author(s):  
Eleni Rebelos ◽  
Brenno Astiarraga ◽  
Roberto Bizzotto ◽  
Andrea Mari ◽  
Maria Laura Manca ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Release ◽  
Cell Function ◽  
Fasting Glucose ◽  
Insulin Resistant ◽  
Esterified Fatty Acids ◽  
Β Cell Function ◽  
Glucose Sensitivity ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Previous work has shown that potentiation of insulin release is impaired in non-diabetic insulin resistance; we tested the hypothesis that this defect may be related to altered glucagon-like peptide-1 (GLP-1) release. On consecutive days, 82 non-diabetic individuals, classified as insulin sensitive (IS, n=41) or insulin resistant (IR, n=41) by the euglycaemic clamp, were given two sequential mixed meals with standard (75 g, LCD) or double (150 g, HCD) carbohydrate content. Plasma glucose, insulin, C-peptide, non-esterified fatty acids (NEFA) and GLP-1 concentrations were measured; β-cell function (glucose sensitivity and potentiation) was resolved by mathematical modelling. Fasting GLP-1 levels were higher in IR than IS (by 15%, P=0.006), and reciprocally related to insulin sensitivity after adjustment for sex, age, fat mass, fasting glucose or insulin concentrations. Mean postprandial GLP-1 responses were tightly correlated with fasting GLP-1, were higher for the second than the first meal, and higher in IR than IS subjects but only with LCD. In contrast, incremental GLP-1 responses were higher during (i) the second than the first meal, (ii) on HCD than LCD, and (iii) significantly smaller in IR than IS independently of meal and load. Potentiation of insulin release was markedly reduced in IR vs IS across meal and carbohydrate loading. In the whole dataset, incremental GLP-1 was directly related to potentiation, and both were inversely related to mean NEFA concentrations. We conclude that (a) raised GLP-1 tone may be inherently linked with a reduced GLP-1 response and (b) defective post-meal GLP-1 response may be one mechanism for impaired potentiation of insulin release in insulin resistance.

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