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 Peak Growth Hormone-Releasing Hormone-Arginine-Stimulated Growth Hormone Is Inversely Associated with Intramyocellular and Intrahepatic Lipid Content in Premenopausal Women with Obesity

2009 ◽  
Vol 94 (10) ◽  
pp. 3995-4002 ◽  
Author(s):  
Miriam A. Bredella ◽  
Martin Torriani ◽  
Bijoy J. Thomas ◽  
Reza Hosseini Ghomi ◽  
Danielle J. Brick ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Growth Hormone ◽  
Premenopausal Women ◽  
Normal Weight ◽  
Visceral Adiposity ◽  
Gh Secretion ◽  
The Metabolic Syndrome ◽  
Intrahepatic Lipids ◽  
Peak Growth Hormone

Context: Visceral adiposity is a strong determinant of GH secretion, and low endogenous GH secretion is associated with increased insulin resistance, a key component of the metabolic syndrome. Increased fat accumulation in skeletal muscle and liver may play an etiological role in the development of insulin resistance and other complications of the metabolic syndrome. Little is known about the role of decreased endogenous GH secretion in the pathogenesis of insulin resistance in obesity. Objective: To investigate the relationship between intramyocellular lipids (IMCL), intrahepatic lipids, and peak-stimulated GH in premenopausal women with obesity. Design and Setting: We conducted a cross-sectional study at a clinical translational research center. Patients: Patients included 21 premenopausal women with obesity (mean body mass index, 34.0 ± 4.5 kg/m2) and 17 normal-weight controls (mean body mass index, 21.9 ± 2.0 kg/m2) of comparable mean age. Main Outcomes Measures: IMCL and intrahepatic lipids were measured with proton magnetic resonance spectroscopy (1H-MRS). Body composition was measured with magnetic resonance imaging. Peak GH was measured after stimulation with GHRH-arginine. Results: Obese subjects had higher IMCL, intrahepatic lipids, abdominal and thigh fat, and thigh muscle mass compared with normal-weight controls. There were strong inverse associations between peak GH and both IMCL and intrahepatic lipids independent of age and visceral adiposity. There were positive associations between IMCL and intrahepatic lipids with measures of insulin resistance and serum triglycerides. Conclusion: In premenopausal women with obesity, peak GH is inversely associated with IMCL and intrahepatic lipids independent of age and visceral adiposity. This suggests that low GH may contribute to insulin resistance in obesity through effects on muscle and intrahepatic lipids. Peak growth hormone after GHRH-arginine stimulation is inversely associated with intramyocellular and intrahepatic lipids in premenopausal women with obesity.

Glucose homeostasis in abdominal obesity: hepatic hyperresponsiveness to growth hormone action

2004 ◽  
Vol 287 (1) ◽  
pp. E63-E68 ◽  
Author(s):  
M. M. Buijs ◽  
J. A. Romijn ◽  
J. Burggraaf ◽  
M. L. de Kam ◽  
M. Frölich ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Glucose Metabolism ◽  
Abdominal Obesity ◽  
Glucose Homeostasis ◽  
Premenopausal Women ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Normal Weight ◽  
Obese Women ◽  
Gh Secretion

It has been suggested that (abdominally) obese individuals are hypersensitive to growth hormone (GH) action. Because GH affects glucose metabolism, this may impact glucose homeostasis in abdominal obesity. Therefore, we studied the effect of GH on glucose metabolism in abdominally obese (OB) and normal-weight (NW) premenopausal women. A 1-h intravenous infusion of GH or placebo was randomly administered to six NW [body mass index (BMI) 21.1 ± 1.9 kg/m2] and six OB (BMI 35.5 ± 1.5 kg/m2) women in a crossover design. Insulin, glucagon, and GH secretion were suppressed by concomitant infusion of somatostatin. Glucose kinetics were measured using a 10-h infusion of [6,6-2H2]glucose. In both groups, similar physiological GH peaks were reached by infusion of GH. GH strongly stimulated endogenous glucose production (EGP) in both groups. The percent increase was significantly greater in OB than in NW women (29.8 ± 11.3 vs. 13.3 ± 7.4%, P = 0.014). Accordingly, GH responsiveness, defined as the maximum response of EGP per unit GH, was increased in OB vs. NW subjects (6.0 ± 2.1 vs. 2.2 ± 1.5 μmol·min−1·mU−1·l−1, P = 0.006). These results suggest that the liver is hyperresponsive to GH action in abdominally obese women. The role of the somatotropic ensemble in the control of glucose homeostasis in abdominal obesity is discussed.

scholarly journals Plasma Gamma-Glutamyltransferase Is Strongly Determined by Acylation Stimulating Protein Levels Independent of Insulin Resistance in Patients with Acute Coronary Syndrome

2013 ◽  
Vol 35 ◽  
pp. 155-161 ◽  
Author(s):  
Jumana Saleh ◽  
Hatem Farhan ◽  
Ibtisam Al-Saqri ◽  
Bashair Al-Riyami ◽  
Katherine Cianflone
Keyword(s):  
Insulin Resistance ◽  
Acute Coronary Syndrome ◽  
Cardiovascular Risk ◽  
Liver Enzymes ◽  
Metabolic Risk ◽  
Risk Markers ◽  
Gamma Glutamyltransferase ◽  
Coronary Syndrome ◽  
The Metabolic Syndrome ◽  
Acylation Stimulating Protein

Background.Steatosis is a manifestation of the metabolic syndrome often associated with release of liver enzymes and inflammatory adipocytokines linked to cardiovascular risk. Gamma-glutamyltransferase (GGT) is one sensitive liver marker recently identified as an independent cardiovascular risk factor. Mechanisms involved in enhanced hepatic lipogenesis causing steatosis are not yet identified and are usually linked to insulin resistance (IR). Acylation stimulating protein (ASP), a potent lipogenic factor, was recently shown to increase in patients with steatosis and was implicated in its pathogenesis.Aim.To investigate the association of plasma ASP levels with liver and metabolic risk markers in acute coronary syndrome (ACS) patients.Methods.28 patients and 30 healthy controls were recruited. Their anthropometrics, lipid profile, liver markers, insulin, and ASP levels were measured.Results.In the patients, ASP, liver, and metabolic risk markers were markedly higher than in the controls. ASP strongly predicted GGT levels (B=0.75,P<0.0001), followed by triglycerides (B=0.403,P=0.017), together determining 57.6% variation in GGT levels. Insulin and IR correlated with metabolic risk components but not with liver enzymes.Conclusion.The strong association of ASP with GGT in ACS patients suggests that ASP, independent of IR, may contribute to a vicious cycle of hepatic lipogenic stimulation and GGT release promoting atherogenesis.

scholarly journals Growth Hormone Deficiency by Growth Hormone Releasing Hormone-Arginine Testing Criteria Predicts Increased Cardiovascular Risk Markers in Normal Young Overweight and Obese Women

2008 ◽  
Vol 93 (7) ◽  
pp. 2507-2514 ◽  
Author(s):  
Andrea L. Utz ◽  
Ami Yamamoto ◽  
Linda Hemphill ◽  
Karen K. Miller
Keyword(s):  
Growth Hormone ◽  
Cardiovascular Risk ◽  
Waist Circumference ◽  
Density Lipoprotein ◽  
Intercellular Adhesion Molecule ◽  
Risk Markers ◽  
Obese Women ◽  
Intercellular Adhesion Molecule 1 ◽  
Tnf Α ◽  
Soluble Intercellular Adhesion Molecule

Abstract Context: Little is known about the relationship between GH and cardiovascular risk markers in women without organic hypothalamic/pituitary disease. Objective: The objective of the study was to determine whether healthy young overweight and obese women, who would be classified as having GH deficiency (GHD) based on standard criteria used in hypopituitarism (peak GH after stimulation with GHRH and arginine &lt; 5 ng/ml), have increased cardiovascular risk markers. Design: This was a cross-sectional study. Setting: The study was conducted at the General Clinical Research Center. Study Participants: Forty-five women of reproductive age, mean age 33.1 ± 1.2 yr and mean body mass index (BMI) 30.9 ± 1.0 kg/m2. Intervention: There was no intervention. Main Outcome Measures: Measures included carotid intima-medial thickness, high-sensitivity C-reactive protein (hsCRP), total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein, triglycerides, E-selectin, soluble intercellular adhesion molecule-1, TNF-α receptor I, TNF-α receptor II, fasting insulin levels, and oral glucose tolerance testing. Results: Twenty-six percent of overweight or obese subjects and none with BMI less than 25 kg/m2 met criteria for GHD. Subjects who met GHD criteria had a mean BMI of 37.0 ± 1.7 kg/m2 (range 28.6–43.6 kg/m2), and their mean waist circumference (110.1 ± 3.5 cm) was higher than in overweight/obese women with GH sufficiency (P = 0.007). Mean carotid intima-media thickness, hsCRP, soluble intercellular adhesion molecule-1, TNF-α receptor I, and TNF-α receptor II levels were higher, and HDL lower, in women meeting GHD criteria than in GH sufficiency. Differences in HDL, hsCRP, and TNF-α receptor II remained after controlling for age plus BMI, waist circumference, or trunk fat. There were no differences in measures of insulin resistance. Conclusions: There may be a relative GHD syndrome in overweight and obese women without organic pituitary or hypothalamic disease that confers increased cardiovascular risk, independent of weight.

scholarly journals Very similar cardiometabolic profile in the moderate and high cardiovascular risk classes: a population-based study

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
M Chlabicz ◽  
J Jamolkowski ◽  
W Laguna ◽  
P Sowa ◽  
M Paniczko ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Cardiovascular Risk ◽  
High Risk ◽  
Population Based ◽  
Low Risk ◽  
Public Institution ◽  
Population Based Study ◽  
The Metabolic Syndrome ◽  
Cardiometabolic Profile

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): Medical University of Bialystok, Poland Background Cardiovascular disease (CVD) is a major, worldwide problem and remain the dominant cause of premature mortality in the word. Simultaneously the metabolic syndrome is a growing problem. The aim of this study was to investigate the cardiometabolic profile among cardiovascular risk classes, and to estimate CV risk using various calculators. Methods The longitudinal, population-based study, was conducted in 2017-2020. A total of 931 individuals aged 20-79 were included. Anthropometric and biochemical profiles were measured according to a standardized protocols. The study population was divided into CV risk classes according to the latest recommendation. Comparisons variables between subgroups were conducted using Dwass-Steele-Critchlow-Fligner test. To estimate CV risk were used: the  Systematic Coronary Risk Estimation system, Framingham Risk Score and LIFEtime-perspective model for individualizing CardioVascular Disease prevention strategies in apparently healthy people (LIFE-CVD). Results The mean age was 49.1± 15.5 years, 43.2% were male. Percentages of low-risk, moderate-risk, high-risk and very-high CV risk were 46.1%, 22.8%, 13.5%, 17.6%, respectively. Most of the analyzed anthropometric, body composition and laboratory parameters did not differ between the moderate and high CV risk participants, whereas the low risk group differed significantly. In the moderate and high-risk groups, abdominal distribution of adipose tissue dominated with significantly elevated parameters of insulin resistance. Interestingly, estimating lifetime risk of myocardial infarction, stroke or CV death using LIFE-CVD calculator yielded similar results in moderate and high CV risk classes. Conclusion The participants belonging to moderate and high CV risk classes have a very similar unfavorable cardiometabolic profile which may result in the similar lifetime CV risk. This may imply the need for more aggressive pharmacological and non-pharmacological management of CV risk factors in the moderate CV risk population. It would be advisable to consider combining the moderate and high risk classes into one high CV risk class, or it may be worth adding one of the parameters of abdominal fat distribution to the CV risk calculators as an expression of increased insulin resistance. Abstract Figure 1.

scholarly journals The Metabolic Syndrome, Insulin Resistance, and Cardiovascular Risk in Diabetic and Nondiabetic Patients

2005 ◽  
Vol 90 (10) ◽  
pp. 5698-5703 ◽  
Author(s):  
Christoph H. Saely ◽  
Stefan Aczel ◽  
Thomas Marte ◽  
Peter Langer ◽  
Guenter Hoefle ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Cardiovascular Risk ◽  
The Metabolic Syndrome

Abstract P347: Serum 25-hydroxy Vitamin D, Cardiovascular Risk Markers, And Incident Myocardial Infarction In A High Risk Community Population

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Jaeun Yang ◽  
Christopher Naugler ◽  
Lawrence de Koning
Keyword(s):  
Myocardial Infarction ◽  
Vitamin D ◽  
Cardiovascular Risk ◽  
High Risk ◽  
Ldl Cholesterol ◽  
Fasting Glucose ◽  
Hdl Cholesterol ◽  
Risk Markers ◽  
25 Oh Vitamin D

Background: It is unclear whether vitamin D deficiency is associated with a higher risk of cardiovascular disease, and through what biochemical pathways this could occur. We investigated the relationship between serum 25-OH vitamin D and typical cardiovascular risk markers as well as incident myocardial infarction (MI) in a large group of high-risk individuals from the community of Calgary, Alberta, Canada. Methods: Calgary Laboratory Services databases were queried for age, sex, body mass index (BMI), personal healthcare number (PHN) and first available serum 25-OH vitamin D measure from patients who received an electrocardiogram or urine creatinine clearance test from 2010-2013. Data was linked by PHN to first available laboratory results for total cholesterol, HDL cholesterol, triglycerides, LDL cholesterol, fasting glucose and HbA1c as well as Alberta Health Services hospital discharge data for first myocardial infarction (ICD-10: I21.1-9) occurring after 25-OH vitamin D measurement. Multiple linear and logistic regression were used to examine all associations. Results: There were 36 000-50 000 complete patient records for analysis of each of the risk markers, with a median follow-up of 8-11 months. A 30 mmol/L increase in serum 25-OH vitamin D was associated with significantly (p<0.001) lower total cholesterol (-0.07 mmol/L), LDL cholesterol (-0.06 mmol/L), triglycerides (-0.14 mmol/L), fasting glucose (-0.12 mmol/L), and HbA1c (-0.13% mmol/L), but higher HDL cholesterol (+0.06 mmol/L) after adjusting for age, sex, BMI, monthly hours of sun-exposure and time between measures. Among these individuals, there were 458 cases of MI occurring after 25-OH vitamin D measurement, with a median follow-up of 1 year. In a case-cohort analysis that included 2500 controls, a 30 mmol/L increase in 25-OH vitamin D was associated with a 21% (p<0.001) lower odds of MI after multivariate adjustment. This association was strongly attenuated after adjusting LDL, HDL, fasting glucose and HbA1c. Conclusion: In a high-risk group of community patients from Calgary, Alberta, Canada, higher serum 25-OH vitamin D was associated with a lower risk of MI, which was explained by changes in commonly measured cardiovascular risk markers. Further study is needed to determine whether changes in cardiovascular risk markers are causally related to changes in 25-OH vitamin D.

scholarly journals Obesity and Insulin Resistance Are the Main Determinants of Postprandial Lipoprotein Dysmetabolism in Polycystic Ovary Syndrome

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Tommy Kyaw Tun ◽  
Anne McGowan ◽  
Niamh Phelan ◽  
Neuman Correia ◽  
Gerard Boran ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Polycystic Ovary Syndrome ◽  
Apolipoprotein B ◽  
Polycystic Ovary ◽  
Density Lipoprotein ◽  
Premenopausal Women ◽  
Postprandial Glucose ◽  
Ovary Syndrome ◽  
Mixed Meal

Postprandial dyslipidaemia may be a plausible mechanism by which polycystic ovary syndrome (PCOS) increases cardiovascular risk. We sought to investigate whether the postprandial glucose and insulin and lipid and lipoprotein responses, including that of apolipoprotein B-48 (apoB-48) containing chylomicrons, to a mixed meal are different in obese PCOS women when compared to obese control subjects and whether differences, if any, are related to obesity, insulin resistance (IR), hyperandrogenaemia, or PCOS status. 26 women with PCOS (age30.4±1.2years (mean ± SEM), body mass index (BMI)36.8±1.5 kg/m2) and 26 non-PCOS subjects (age34.1±0.9years, BMI31.5±1.0 kg/m2) were studied before and up to 8 hours following a standard mixed meal. AUC-triglyceride (AUC-TG) was higher and AUC-high-density lipoprotein (AUC-HDL) lower in PCOS women. These differences were not apparent when BMI was accounted for. Insulin sensitivity (SI), AUC-apoB-48, and AUC-apolipoprotein B (AUC-apoB) were found to be independent predictors of AUC-TG, accounting for 55% of the variance. Only AUC-insulin remained significantly elevated following adjustment for BMI. Obesity related IR explains postprandial hypertriglyceridaemia and hyperinsulinaemic responses. Management of obesity in premenopausal women with PCOS is likely to reduce their cardiovascular risk burden.

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