Abstract 623: Angiotensin Receptor Activation Contributes to Glucose Intolerance and Increased Insulin Resistance Independent of Elevated Systolic Blood Pressure, Adiposity and Dyslipidemia in a Model of Metabolic Syndrome

Activation of the renin-angiotensin system (RAS) leads to an increase in blood pressure and onset of insulin resistance (IR); however, the contributions of increased blood pressure and AT1 activation independently on the manifestation of IR are not well defined. The goal of this study was to determine the contribution of elevated blood pressure, independent of RAS, to the onset of IR in a model of metabolic syndrome. To address the hypothesis that AT1 activation, and not elevated blood pressure independently, is the principal contributor of obesity-associated IR, we measured changes in systolic blood pressure (SBP), adiposity, plasma triglycerides (TG), glucose tolerance, and insulin resistance index (IRI) in four groups of rats: 1) lean strain-control Long Evans Tokushima Otsuka (LETO; n=5), 2) obese Otsuka Long-Evans Tokushima Fatty (OLETF; n=7), 3) OLETF + angiotensin receptor blocker (ARB; 10 mg olmesartan/kg; n=8), and 4) OLETF + calcium channel blocker (CCB; 5 mg amlodipine/kg; n=7). ARB treatment alleviated the obesity-related increase in mean SBP, while the decrease with CCB remained 10.2 mmHg greater than LETO. ARB (0.51 g/100g body mass) and CCB (0.64 g/100g body mass) reduced mean relative retroperitoneal fat mass and mean plasma triglycerides (28.4 and 27.4 mg/dL respectively) compared to OLETF, but both remained greater (1.7, 1.57 g/100g body mass and 28.94, 29.94 mg/dL respectively) than LETO. ARB improved glucose tolerance by 4605.94 of 34965.94 and mean calculated IRI by 5581429.5 of 17398363, but CCB had no detectable effect on either. Despite relatively similar reductions in SBP, adiposity and plasma TG (principal components of metabolic syndrome), CCB did not improve glucose tolerance and IRI (additional metrics of metabolic syndrome), while ARB did, demonstrating that AT1 activation is the primary factor contributing to the development of impaired glucose metabolism and regulation during metabolic syndrome, independent of the hypertension, adiposity and dyslipidemia. Thus, targeting RAS to improve the consequences of metabolic syndrome appears to be prudent and effective.

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The effects of metformin plus sulfonylurea therapy on clinical features of the metabolic syndrome

Medicinski pregled ◽

10.2298/mpns1010611k ◽

2010 ◽

Vol 63 (9-10) ◽

pp. 611-615 ◽

Cited By ~ 1

Author(s):

Branka Koprivica ◽

Teodora Beljic-Zivkovic ◽

Tatjana Ille

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Type 2 Diabetes ◽

Metabolic Syndrome ◽

Body Mass Index ◽

Waist Circumference ◽

Glycemic Control ◽

Body Mass ◽

Combined Therapy

Introduction. Insulin resistance is a well-known leading factor in the development of metabolic syndrome. The aim of this study was to evaluate metabolic effects of metformin added to sulfonylurea in unsuccessfully treated type 2 diabetic patients with metabolic syndrome. Material and methods. A group of thirty subjects, with type 2 diabetes, secondary sulfonylurea failure and metabolic syndrome were administered the combined therapy of sulfonylurea plus metformin for six months. Metformin 2000 mg/d was added to previously used sulfonylurea agent in maximum daily dose. Antihypertensive and hypolipemic therapy was not changed. The following parameters were assessed at the beginning and after six months of therapy: glycemic control, body mass index, waist circumference, blood pressure, triglycerides, total cholesterol and its fractions, homeostatic models for evaluation of insulin resistance and secretion (HOMA R, HOMA B) and C- peptide. Results. Glycemic control was significantly improved after six months of the combined therapy: (fasting 7.89 vs. 10.61 mmol/l. p<0.01; postprandial 11.12 vs. 12.61 mmol/l. p<0.01, p<0.01; glycosylated hemoglobin 6.81 vs. 8.83%. p<0.01). the body mass index and waist circumference were significantly lower (26.7 vs. 27.8 kg/m2, p<0.01 and 99.7 vs. 101.4 cm for men, p<0.01; 87.2 vs. 88.5 for women, p<0.01). Fasting plasma triglycerides decreased from 3.37 to 2.45 mmol/l (p<0.001) and HOMA R from 7.04 to 5.23 (p<0.001). No treatment effects were observed on blood pressure, cholesterol, and residual insulin secretion. Conclusion. Administration of metformin in type 2 diabetes with metabolic syndrome decreased cardiovascular risk factors by reducing glycemia, triglycerides, BMI, central obesity and insulin resistance.

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Na+-sensitive elevation in blood pressure is ENaC independent in diet-induced obesity and insulin resistance

AJP Renal Physiology ◽

10.1152/ajprenal.00265.2015 ◽

2016 ◽

Vol 310 (9) ◽

pp. F812-F820 ◽

Cited By ~ 16

Author(s):

Jonathan M. Nizar ◽

Wuxing Dong ◽

Robert B. McClellan ◽

Mariana Labarca ◽

Yuehan Zhou ◽

...

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Elevated Blood Pressure ◽

Elevated Blood ◽

High Fat ◽

Electrolyte Excretion ◽

Diet Induced Obesity ◽

Collecting Ducts ◽

Fat Feeding

The majority of patients with obesity, insulin resistance, and metabolic syndrome have hypertension, but the mechanisms of hypertension are poorly understood. In these patients, impaired sodium excretion is critical for the genesis of Na+-sensitive hypertension, and prior studies have proposed a role for the epithelial Na+ channel (ENaC) in this syndrome. We characterized high fat-fed mice as a model in which to study the contribution of ENaC-mediated Na+ reabsorption in obesity and insulin resistance. High fat-fed mice demonstrated impaired Na+ excretion and elevated blood pressure, which was significantly higher on a high-Na+ diet compared with low fat-fed control mice. However, high fat-fed mice had no increase in ENaC activity as measured by Na+ transport across microperfused cortical collecting ducts, electrolyte excretion, or blood pressure. In addition, we found no difference in endogenous urinary aldosterone excretion between groups on a normal or high-Na+ diet. High fat-fed mice provide a model of metabolic syndrome, recapitulating obesity, insulin resistance, impaired natriuresis, and a Na+-sensitive elevation in blood pressure. Surprisingly, in contrast to previous studies, our data demonstrate that high fat feeding of mice impairs natriuresis and produces elevated blood pressure that is independent of ENaC activity and likely caused by increased Na+ reabsorption upstream of the aldosterone-sensitive distal nephron.

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Consumption of added sugars and development of metabolic syndrome components among a sample of youth at risk of obesity

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2013-0456 ◽

2014 ◽

Vol 39 (4) ◽

pp. 512-512 ◽

Cited By ~ 12

Author(s):

JiaWei Wang

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Glucose Tolerance ◽

Fat Mass ◽

Diet Quality ◽

Healthy Eating Index ◽

Added Sugar ◽

Added Sugars ◽

Sugar Intake

Previous evidence showed controversial links between added sugar intake, diet quality, and increasing prevalence of metabolic syndrome (MetS) components (abdominal adiposity, dysglycemia, elevated blood pressure, reduced high-density lipoprotein cholesterol (HDL-C), and hypertriglyceridemia) in youth, and most studied only its liquid source of sugar-sweetened beverages (SSB). To better understand the extent of the detrimental effects of added sugars from both liquid and solid sources to diets in terms of nutrient and food intake and metabolic consequences in children, 3 studies were undertaken to (i) quantify the associations of added sugar intake with overall diet quality and adiposity indicators; (ii) assess whether excess weight and glucose tolerance status modifies the associations between consumption of added sugars and MetS components; and (iii) evaluate whether consumption of added sugars predicts the development of MetS components over time. Data for these studies were obtained from the Quebec Adiposity and Lifestyle Investigation in Youth cohort. Caucasian children (8 to 10 years at baseline, N = 630) with at least 1 obese biological parent were recruited from 1040 Quebec primary schools and followed-up 2 years later (N = 564). Dietary intake, including added sugars (liquid vs. solid) and Canadian Healthy Eating Index (HEI-C) was assessed in three 24-h recalls at baseline. Adiposity indicators included measured height and weight for body mass index (BMI), BMI z score, waist circumference (WC), and fat mass (by dual-energy X-ray absorptiometry). Plasma glucose and insulin were measured at fasting and by oral glucose tolerance tests to calculate the homeostasis model assessment of insulin resistance (HOMA-IR) and the Matsuda IS index (Matsuda-ISI). Systolic blood pressure (SBP), concentration of triglycerides and HDL-C were measured by standard instruments. Multivariate linear regression models were used, adjusting for age, sex, pubertal status (by Tanner stage), energy intake, fat mass, and physical activity (by 7-day accelerometer). The main findings include the following: (i) Higher consumption of added sugars from SSB or solid sources was associated with lower nutrient density and lower HEI-C. Positive associations with adiposity indicators were observed with consumption of added sugars from liquid sources only. (ii) Higher SSB consumption was associated with higher HOMA-IR and higher SBP among overweight children (≥85th BMI percentile), as well as higher SBP and higher WC among children with impaired glucose tolerance. These associations with metabolic indicators were not observed among children whose BMI was below 85th percentile. (iii) No association with added sugar intake was observed for 2-year changes in adiposity, but higher consumption of added sugars from liquid sources was associated with higher fasting glucose, higher fasting insulin, higher HOMA-IR, and lower Matsuda-ISI. In conclusion, this thesis suggested that consumption of added sugars from both solid and liquid sources was associated with a lower overall diet quality, but only added sugars from liquid sources was associated with adiposity indicators. Cross-sectional links with higher levels of SSB intake and MetS components were more evident among overweight/obese and glucose-intolerant children. Consumption of added sugars from liquid sources was not associated with changes in adiposity over 2 years, but was clearly associated with development of impaired glucose homeostasis and insulin resistance. This thesis presents further evidence on the nutritional and metabolic consequences of consuming added sugar from liquid and solid sources.

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High TSH Level within Normal Range Is Associated with Obesity, Dyslipidemia, Hypertension, Inflammation, Hypercoagulability, and the Metabolic Syndrome: A Novel Cardiometabolic Marker

Journal of Clinical Medicine ◽

10.3390/jcm8060817 ◽

2019 ◽

Vol 8 (6) ◽

pp. 817 ◽

Cited By ~ 8

Author(s):

Yi-Cheng Chang ◽

Shih-Che Hua ◽

Chia-Hsuin Chang ◽

Wei-Yi Kao ◽

Hsiao-Lin Lee ◽

...

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Central Obesity ◽

Cardiometabolic Risk ◽

Fasting Glucose ◽

Reference Group ◽

Elevated Blood ◽

Normal Range ◽

The Metabolic Syndrome

(1) Background: Overt and subclinical hypothyroidism has been associated with increased cardiometabolic risks. Here we further explore whether thyroid function within normal range is associated with cardiometabolic risk factors in a large population-based study. (2) Methods: We screened 24,765 adults participating in health examinations in Taiwan. Participants were grouped according to high-sensitive thyroid-stimulating hormone (hsTSH) level as: <50th percentile (0.47–1.48 mIU/L, the reference group), 50–60th percentile (1.49–1.68 mIU/L), 60–70th percentile (1.69–1.94 mIU/L), 70–80th percentile (1.95–2.3 mIU/L), 80–90th percentile (2.31–2.93 mIU/L), and >90th percentile (>2.93 mIU/L). Cardiometabolic traits of each percentile were compared with the reference group. (3) Results: Elevated hsTSH levels within normal range were dose-dependently associated with increased body mass index, body fat percentage, waist circumferences, blood pressure, hemoglobin A1c (HbA1c), fasting insulin, homeostasis model assessment of insulin resistance (HOMA-IR), high homeostasis model of assessment of beta-cell (HOMA-β), triglycerides, total cholesterols, fibrinogen, and uric acids (p-for-trend <0.001), but not with fasting glucose levels. The association remained significant after adjustment of age, sex, and lifestyle. As compared to the reference group, subjects with the highest hsTSH percentile had significantly increased risk of being overweight (adjusted odds ratio (adjOR): 1.35), increased body fat (adjOR: 1.29), central obesity (adjOR: 1.36), elevated blood pressure (adjOR: 1.26), high HbA1c (adjOR: 1.20), hyperinsulinemia (adjOR: 1.75), increased HOMA-IR (adjOR: 1.45), increased HOMA-β (adjOR: 1.40), hypertriglyceridemia (adjOR: 1.60), hypercholesterolemia (adjOR: 1.25), elevated hsCRP (adjOR: 1.34), increased fibrinogen (adjOR: 1.45), hyperuricemia (adjOR: 1.47), and metabolic syndrome (adjOR: 1.42), but significant risk of low fasting glucose (adjOR: 0.89). Mediation analysis indicates that insulin resistance mediates the majority of the association between thyroid hormone status and the metabolic syndrome. (4) Conclusion: Elevated hsTSH within the normal range is a cardiometabolic risk marker associated with central obesity, insulin resistance, elevated blood pressure, dyslipidemia, hyperuricemia, inflammation, and hypercoagulability.

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Biology of metabolic syndrome in a vascular patient

Vascular ◽

10.1258/vasc.2011.201201 ◽

2012 ◽

Vol 20 (3) ◽

pp. 156-165 ◽

Cited By ~ 7

Author(s):

Daynene Vykoukal ◽

Mark G Davies

Keyword(s):

Risk Factors ◽

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Fasting Blood Glucose ◽

Adverse Impact ◽

Atherogenic Dyslipidemia ◽

Elevated Blood ◽

Vascular Beds ◽

Vascular Patient

Metabolic syndrome is highly prevalent in vascular patients and has a significant impact on the outcomes of vascular interventions. It comprises of a set of metabolically driven risk factors, including truncal obesity, dyslipidemia, elevated blood pressure and elevated fasting blood glucose. Increased insulin resistance within the context of obesity and hypertension contributes to atherogenic dyslipidemia, hyperglycemia, and prothrombotic and proinflammatory states which lead to the adverse impact of metabolic syndrome on the response to injury and on atherosclerotic disease progression. This review focuses on the complex biology of metabolic syndrome and its relevance to management of vascular patients, including outcomes and implications for the coronary, cerebrovascular and lower-extremity vascular beds.

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Insulin infusion induces endothelin-1-dependent hypertension in rats

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00536.2003 ◽

2004 ◽

Vol 287 (5) ◽

pp. E948-E954 ◽

Cited By ~ 24

Author(s):

Chi-Chang Juan ◽

Yi-Wen Shen ◽

Yueh Chien ◽

Yen-Jie Lin ◽

Shau-Feng Chang ◽

...

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Insulin Sensitivity ◽

Glucose Tolerance ◽

Systolic Blood Pressure ◽

Insulin Infusion ◽

Experimental Period ◽

Oral Glucose ◽

Oral Glucose Tolerance ◽

Bq 610

We previously showed that chronic insulin infusion induces insulin resistance, hyperendothelinemia, and hypertension in rats (C. C. Juan, V. S. Fang, C. F. Kwok, J. C. Perng, Y. C. Chou, and L. T. Ho. Metabolism 48: 465–471, 1999). Endothelin-1 (ET-1), a potent vasoconstrictor, is suggested to play an important role in maintaining vascular tone and regulating blood pressure, and insulin increases ET-1 production in vivo and in vitro. In the present study, BQ-610, a selective endothelin A receptor antagonist, was used to examine the role of ET-1 in insulin-induced hypertension in rats. BQ-610 (0.7 mg/ml; 0.5 ml/kg body wt) or normal saline was given intraperitoneally two times daily for 25 days to groups of rats infused with either saline or insulin (2 U/day via sc-implanted osmotic pumps), and changes in plasma levels of insulin, glucose, and ET-1 and the systolic blood pressure were measured over the experimental period, whereas changes in insulin sensitivity were examined at the end of the experimental period. Plasma insulin and ET-1 levels were measured by RIA, plasma glucose levels using a glucose analyzer, systolic blood pressure by the tail-cuff method, and insulin sensitivity by an oral glucose tolerance test. Our studies showed that insulin infusion caused sustained hyperinsulinemia in both saline- and BQ-610-injected rats over the infusion period. After pump implantation (2 wk), the systolic blood pressure was significantly higher in insulin-infused rats than in saline-infused rats in the saline-injected group (133 ± 3.1 vs. 113 ± 1.1 mmHg, P < 0.05) but not in the BQ-610-injected group (117 ± 1.2 vs. 117 ± 1.8 mmHg). Plasma ET-1 levels in both sets of insulin-infused rats were higher than in saline-infused controls (2.5 ± 0.6 and 2.5 ± 0.8 vs. 1.8 ± 0.4 and 1.7 ± 0.3 pmol/l, P < 0.05). Oral glucose tolerance tests showed that BQ-610 treatment did not prevent the insulin resistance caused by chronic insulin infusion. No significant changes were found in insulin sensitivity and blood pressure in saline-infused rats treated with BQ-610. In a separate experiment, insulin infusion induced the increase in arterial ET-1 content, hypertension, and subsequent plasma ET-1 elevation in rats. These results suggest that, in the insulin infusion rat model, ET-1 plays a mediating role in the development of hypertension, but not of insulin resistance.

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Angiotensin receptor-mediated oxidative stress is associated with impaired cardiac redox signaling and mitochondrial function in insulin-resistant rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00101.2013 ◽

2013 ◽

Vol 305 (4) ◽

pp. H599-H607 ◽

Cited By ~ 35

Author(s):

José Pablo Vázquez-Medina ◽

Irina Popovich ◽

Max A. Thorwald ◽

Jose A. Viscarra ◽

Ruben Rodriguez ◽

...

Keyword(s):

Oxidative Stress ◽

Insulin Resistance ◽

Metabolic Syndrome ◽

Protein Expression ◽

Mitochondrial Function ◽

Citrate Synthase ◽

Cellular Metabolism ◽

Redox Signaling ◽

Angiotensin Receptor ◽

Long Evans

Activation of angiotensin receptor type 1 (AT1) contributes to NADPH oxidase (Nox)-derived oxidative stress during metabolic syndrome. However, the specific role of AT1 in modulating redox signaling, mitochondrial function, and oxidative stress in the heart remains more elusive. To test the hypothesis that AT1 activation increases oxidative stress while impairing redox signaling and mitochondrial function in the heart during diet-induced insulin resistance in obese animals, Otsuka Long Evans Tokushima Fatty (OLETF) rats ( n = 8/group) were treated with the AT1 blocker (ARB) olmesartan for 6 wk. Cardiac Nox2 protein expression increased 40% in OLETF compared with age-matched, lean, strain-control Long Evans Tokushima Otsuka (LETO) rats, while mRNA and protein expression of the H2O2-producing Nox4 increased 40–100%. ARB treatment prevented the increase in Nox2 without altering Nox4. ARB treatment also normalized the increased levels of protein and lipid oxidation (nitrotyrosine, 4-hydroxynonenal) and increased the redox-sensitive transcription factor Nrf2 by 30% and the activity of antioxidant enzymes (SOD, catalase, GPx) by 50–70%. Citrate synthase (CS) and succinate dehydrogenase (SDH) activities decreased 60–70%, whereas cardiac succinate levels decreased 35% in OLETF compared with LETO, suggesting that mitochondrial function in the heart is impaired during obesity-induced insulin resistance. ARB treatment normalized CS and SDH activities, as well as succinate levels, while increasing AMPK and normalizing Akt, suggesting that AT1 activation also impairs cellular metabolism in the diabetic heart. These data suggest that the cardiovascular complications associated with metabolic syndrome may result from AT1 receptor-mediated Nox2 activation leading to impaired redox signaling, mitochondrial activity, and dysregulation of cellular metabolism in the heart.

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Fasting alters the gut microbiome reducing blood pressure and body weight in metabolic syndrome patients

Nature Communications ◽

10.1038/s41467-021-22097-0 ◽

2021 ◽

Vol 12 (1) ◽

Cited By ~ 1

Author(s):

András Maifeld ◽

Hendrik Bartolomaeus ◽

Ulrike Löber ◽

Ellen G. Avery ◽

Nico Steckhan ◽

...

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Body Mass Index ◽

T Cells ◽

Regulatory T Cells ◽

Systolic Blood Pressure ◽

Body Mass ◽

Gut Microbiome ◽

Effector T Cells ◽

Pharmacological Intervention

AbstractPeriods of fasting and refeeding may reduce cardiometabolic risk elevated by Western diet. Here we show in the substudy of NCT02099968, investigating the clinical parameters, the immunome and gut microbiome exploratory endpoints, that in hypertensive metabolic syndrome patients, a 5-day fast followed by a modified Dietary Approach to Stop Hypertension diet reduces systolic blood pressure, need for antihypertensive medications, body-mass index at three months post intervention compared to a modified Dietary Approach to Stop Hypertension diet alone. Fasting alters the gut microbiome, impacting bacterial taxa and gene modules associated with short-chain fatty acid production. Cross-system analyses reveal a positive correlation of circulating mucosa-associated invariant T cells, non-classical monocytes and CD4+ effector T cells with systolic blood pressure. Furthermore, regulatory T cells positively correlate with body-mass index and weight. Machine learning analysis of baseline immunome or microbiome data predicts sustained systolic blood pressure response within the fasting group, identifying CD8+ effector T cells, Th17 cells and regulatory T cells or Desulfovibrionaceae, Hydrogenoanaerobacterium, Akkermansia, and Ruminococcaceae as important contributors to the model. Here we report that the high-resolution multi-omics data highlight fasting as a promising non-pharmacological intervention for the treatment of high blood pressure in metabolic syndrome patients.

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Frequency of Metabolic Syndrome and the Role of Radiotherapy in Patients with Acute Lymphoblastic Leukemia Who Completed Therapy.

Blood ◽

10.1182/blood.v114.22.4551.4551 ◽

2009 ◽

Vol 114 (22) ◽

pp. 4551-4551

Author(s):

Yesim Oymak ◽

Aysen Turedi ◽

Yontem Yaman ◽

Muammer Buyukinan ◽

Kaan Kavakli ◽

...

Keyword(s):

Insulin Resistance ◽

Blood Pressure ◽

Metabolic Syndrome ◽

Glucose Tolerance ◽

Impaired Fasting Glucose ◽

Fasting Glucose ◽

Risk Group ◽

Lymphoblastic Leukemia ◽

Risk Groups ◽

Discontinuation Of Treatment

Abstract Abstract 4551 Objective The aim of the study was to evaluate the frequency of metabolic syndrome and its components, and the effect of radiotherapy on the development of metabolic syndrome and its components in patients with acute lymphoblastic leukemia (ALL) who completed therapy. Material method Age of diagnosis, time elapsed since discontinuation of treatment, gender and risk group information were recorded for 40 ALL patients with completed therapy who were enrolled in the study. Height, body weight, systolic and diastolic blood pressure levels, HDL, LDL, triglyceride, total cholesterol, fasting blood sugar (FBS) and insulin levels were determined. The patients' height SDS, body mass index (BMI) and BMI percentiles were calculated. Considering age and gender, patients in the BMI percentile of 85-95 were considered overweight, and patients above the 95 percentile were considered obese. Height SDS < -2 SDS was considered as shortness in height. 90 and 95 p systolic and diastolic blood pressure values by height percentile were taken as basis for the blood pressure assessment. WHO (modified) criteria were used for diagnosing the metabolic syndrome. HOMA-IR > 4 was accepted as insulin resistance for evaluating insulin resistance. Results A total of 40 patients, 24 females and 16 males, were enrolled in the study. Median age was 49 months (16-165), and the median time lapsed since discontinuation of treatment was 12 (1-96) months. 19 of the patients were in the standard risk group (SRG), 18 were in the moderate risk group (MRG), and 3 were in the high risk group (HRG) and 20 patients had received radiotherapy. Seven patients were obese, six patients were overweight, eight patients had insulin resistance, one patient had impaired fasting glucose tolerance, six cases were diagnosed with hypertension, seven with dyslipidemia, and five cases with metabolic syndrome. While no difference was observed in groups that received and did not receive radiotherapy in terms of BMI, HOMA IR, insulin, FBS, triglyceride, LDL, and T cholesterol (p>0.05), the HDL value was observed to be higher in the group which did not receive radiotherapy (p=0.032). No difference could be observed between the two groups in terms of obesity, overweight, impaired fasting glucose tolerance, hypertension, dyslipidemia, and metabolic syndrome parameters. The difference between the radiotherapy and non-radiotherapy groups' mean SDS values (-0.48/-0.23) was not significant. While no difference could be observed in the BMI, HOMA IR, insulin, FBS, triglyceride, LDL, total cholesterol levels of the ALL risk groups (p>0.05), a difference in the HDL value was found among the groups (p<0.05). A difference in obesity, overweight, impaired fasting glucose tolerance, hypertension, dislipidemia, metabolic syndrome among the groups, and a difference in mean height SDS of the groups (-0.23/-0.55/-0.15) could not be found (p>0.05). Three patients had height measurements below -2SDS. A difference could not be observed among the risk groups and between RT and non-RT groups in terms of shortness in height. Discussion A difference could not be observed between the radiotherapy and non-radiotherapy groups in terms of metabolic syndrome. However, the importance of monitoring weight, height, and metabolic parameters during routine controls of children with ALL who completed therapy is once more underlined as metabolic syndrome was seen in 12.5% percent of the study subjects. Disclosures: No relevant conflicts of interest to declare.

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