scholarly journals Microalbuminuria in never-treated hypertensives : relations with left ventricular characteristics, insulin sensitivity and genetic predisposition to hypertension.

1999 ◽  
Vol 12 (4) ◽  
pp. 83
Author(s):  
A GRANDI
Keyword(s):  
Insulin Sensitivity ◽  
Genetic Predisposition ◽  
Left Ventricular

Exercise does not change the differences in insulin sensitivity inherent to the Genetic Predisposition

2013 ◽  
Vol 61 (S 01) ◽  
Author(s):  
M Schwarzer ◽  
A Molis ◽  
A Schrepper ◽  
SL Britton ◽  
LG Koch ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Genetic Predisposition

scholarly journals Takotsubo Syndrome: Contemporary Views on the Pathogenesis, Prevalence and Prognosis

2018 ◽  
Vol 14 (4) ◽  
pp. 598-604 ◽  
Author(s):  
A. S. Shilova ◽  
A. O. Shmotkina ◽  
A. A. Yafarova ◽  
M. Yu. Gilyarov
Keyword(s):  
Genetic Predisposition ◽  
Randomized Clinical Trials ◽  
Myocardial Dysfunction ◽  
Specific Treatment ◽  
Left Ventricular ◽  
Takotsubo Syndrome ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
St Segment ◽  
Reversible Left Ventricular Dysfunction

Takotsubo syndrome (TTS) is a reversible left ventricular dysfunction characterized by local apical hypokinesia usually triggered by a physical or emotional stress. According to the last available data TTS may represent 2% of all admissions for acute coronary syndromes. Despite the reliable prevalence, diagnosis of TTS remains difficult. The initial presentation, both clinically and electrocardiographically, is similar to an acute myocardial infarction (AMI). The biomarker profile is also similar, although the peaks of troponin and creatinine kinase levels are lower, and brain natriuretic peptide levels are higher in patients with TTS compared with ST-segment elevation AMI. Modified Mayo diagnostic criteria are the most common for the diagnosis. Pathogenesis of TTS currently is not well understood. Catecholamines appear to play a central role in the pathophysiology of TTS. However, it is conceivable that some people have a genetic predisposition to stress-induced TTS. A genetic predisposition has been suggested based on the few familial TTS cases described. Despite reversible myocardial dysfunction, acute heart failure is the most common complication in the acute phase of TTS. In-hospital mortality rate is comparable to that of ST-segment elevation AMI. There are no randomized clinical trials to support specific treatment recommendations in TTS. It is believed that the tactics of managing patients with TTS hospitalized with suspicion of acute coronary syndrome should comply with the protocol of management of patients with AMI while acute coronary pathology is not excluded.

scholarly journals Impact of successful transsphenoidal surgery on cardiovascular risk factors in acromegaly

2003 ◽  
pp. 193-201 ◽  
Author(s):  
ML Jaffrain-Rea ◽  
G Minniti ◽  
C Moroni ◽  
V Esposito ◽  
E Ferretti ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Cardiovascular Risk ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Cardiovascular Risk Factors ◽  
Transsphenoidal Surgery ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Igf I

BACKGROUND: Cardiac abnormalities develop in patients with acromegaly as a consequence of effects of GH/IGF-I on the heart and related cardiovascular risk factors. OBJECTIVE: To evaluate the possible contribution of postoperative variations in blood pressure (BP), glucose tolerance and insulin sensitivity to the cardiac improvement reported in patients who have been cured of acromegaly. DESIGN: Thirty-one patients with acromegaly were studied before and 6 Months after successful transsphenoidal surgery, defined by normal age-related IGF-I concentrations and glucose-suppressed GH concentrations <1 microg/l. METHODS: Cardiovascular parameters were assessed by Doppler echocardiography and 24-h ambulatory blood pressure monitoring. Insulin sensitivity indexes were calculated on the basis of fasting and post-load glycaemia and insulinaemia and referred to as HOMA(ISI) and OGTT(ISI), respectively. RESULTS: Successful surgery was confirmed to improve left ventricular mass index (LVMI) and diastolic filling significantly. Mean 24-h systolic BP values decreased (P=0.009) and BP rhythm was restored in 12 of 15 patients with a blunted preoperative profile. Glucose tolerance normalized in patients with preoperative glucose intolerance (n=7) or diabetes mellitus (n=3). HOMA(ISI) and OGTT(ISI) increased (P=0.0001 for each parameter), indicating a marked improvement in insulin sensitivity. The postoperative reduction in LVMI correlated with increased insulin sensitivity (P<0.001 for both indexes), but not with other parameters. Improved diastolic filling correlated with the reduction in LVMI. CONCLUSIONS: Successful surgery in patients with acromegaly induces a significant improvement in haemodynamic and metabolic risk factors. This study suggests a direct link between insulin resistance and acromegalic cardiomyopathy.

scholarly journals 3068 Effects of exercise and a very low fat diet in metabolically abnormal obese adults

2019 ◽  
Vol 3 (s1) ◽  
pp. 40-40
Author(s):  
George Schweitzer ◽  
Monica Kearney ◽  
Gordon Smith ◽  
Samuel Klein
Keyword(s):  
Weight Loss ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Comparative Trial ◽  
Left Ventricular Diastolic Function ◽  
Postprandial Glucose ◽  
Left Ventricular ◽  
Low Fat ◽  
Glucose Response ◽  
Skeletal Muscle Insulin Sensitivity

OBJECTIVES/SPECIFIC AIMS: People with metabolically abnormal obesity (MAO), defined as those with insulin resistance and high intrahepatic triglyceride, are at high risk for developing type 2 diabetes and cardiovascular disease. Weight loss through reduced energy intake and increased physical activity has profound impacts on improving cardiometabolic function. However, the specific additional effects of exercise training with diet-induced weight loss on metabolic function are equivocal. METHODS/STUDY POPULATION: A comparative trial is ongoing in MAO adults undergoing 8-10% weight loss induced by a very-low fat plant-based (PB) diet with structured exercise training (n=8) compared to the same weight loss induced by the PB diet alone (n=3). RESULTS/ANTICIPATED RESULTS: Preliminary results indicate that, PB diet with or without exercise training results in significant weight loss concomitant with enhanced insulin sensitivity, reduced intrahepatic triglyceride, reduced 24-hour postprandial glucose response, reduced fat mass, and reduced diastolic blood pressure. Those undergoing PB diet with exercise training had greater improvements in muscular strength and cardiorespiratory fitness than those undergoing PB diet alone. Differences between intervention groups for other cardiometabolic measures are not yet known. DISCUSSION/SIGNIFICANCE OF IMPACT: Each of the interventions resulted in improved cardiometabolic measures; however the extent of the differences between the interventions is not yet clear. It is hypothesized that compared with weight loss induced by a PB diet, the same weight loss induced by a PB diet and structured exercise training will i) cause greater improvement in skeletal muscle insulin sensitivity, ii) will attenuate the usual decline in muscle mass while increasing strength, and iii) result in greater increases in left ventricular diastolic function. The long-term objective of this proposal is to provide a foundation for future studies evaluating mechanisms for the effects of exercise in cardiometabolic disease prevention and therapy.

scholarly journals Camk2n1 Is a Negative Regulator of Blood Pressure, Left Ventricular Mass, Insulin Sensitivity, and Promotes Adiposity

Hypertension ◽  
2019 ◽  
Vol 74 (3) ◽  
pp. 687-696 ◽  
Author(s):  
Neza Alfazema ◽  
Marjorie Barrier ◽  
Sophie Marion de Procé ◽  
Robert I. Menzies ◽  
Roderick Carter ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Left Ventricular Mass ◽  
Left Ventricular ◽  
Negative Regulator ◽  
Ventricular Mass

Relationship of Left Ventricular Mass to Insulin Sensitivity and Body Mass Index in Healthy Individuals

2006 ◽  
Vol 61 (4) ◽  
pp. 398-406 ◽  
Author(s):  
Haksun EBINÇ ◽  
Fatma Ayerden EBINÇ ◽  
Zübeyde Nur ÖZKURT ◽  
Tolga DOGRU ◽  
Murat YILMAZ
Keyword(s):  
Body Mass Index ◽  
Insulin Sensitivity ◽  
Left Ventricular Mass ◽  
Body Mass ◽  
Left Ventricular ◽  
Healthy Individuals ◽  
Ventricular Mass ◽  
Relationship Of

Abstract 15225: Post-ischemic Myocardial Insulin Resistance Induced by Tnf-α Overproduction Precipitates the Development of Heart Failure After Myocardial Infarction

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Feng Fu ◽  
Jia Li ◽  
Jie Xu ◽  
Yuan Zhang ◽  
Chao Gao ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Insulin Resistance ◽  
Insulin Sensitivity ◽  
Insulin Signaling ◽  
Left Ventricular ◽  
Separate Experiment ◽  
Tnf Α ◽  
Lv Remodeling ◽  
Myocardial Insulin Resistance

Objectives: Clinical evidence has demonstrated a decreased myocardial insulin response in HF patients. However, the role of myocardial insulin resistance and the underlying mechanisms in HF are largely unclear. Methods and Results: Sprague Dawley rats subjected to myocardial infarction (MI) resulted in a progressive left ventricular (LV) remodeling and dysfunction. Echocardiographic assessment showed preserved LV end-systolic dimension (LVESD 0.453 ± 0.027 cm) and ejection fraction (EF 57.03 ± 2.35%) at 1 wk after MI, and evident LV dilation (LVESD 0.612 ± 0.026 cm) and dysfunction (EF 40.21 ± 3.09%) at 4 wk after MI. Myocardial insulin sensitivity decreased significantly at 1 wk after MI as evidenced by reduced insulin-stimulated myocardial fluorodeoxyglucose uptake (Standardized Uptake Value: 2.71 ± 0.42 vs. 5.13 ± 0.51 of sham+insulin, n=6, P <0.01) and GLUT-4 translocation and altered insulin signaling, whereas systemic insulin sensitivity remained unchanged. Mechanistically, myocardial TNF-α production was increased following MI. Treatment with etanercept (a TNF-α inhibitor) post-MI improved myocardial insulin sensitivity, while adenovirus-mediated overexpression of TNF-α resulted in myocardial insulin resistance in non-MI hearts. In addition, TNF-α overexpressed rat hearts exhibited LV dysfunction (EF 41.32 ± 4.21%) and LV dilation as early as 1 wk after MI. Moreover, insulin treatment during the first week following MI suppressed myocardial TNF-α production and increased myocardial insulin sensitivity, resulting in alleviated cardiac dysfunction and remodeling at 4 wk after MI. Importantly, in a separate experiment, cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic LV remodeling and dysfunction compared with littermate controls. Conclusions: Our data provide novel insights that myocardial insulin resistance, independently of systemic insulin resistance, precipitates the development of post-ischemic HF. Myocardial insulin resistance is an early event partly attributed to myocardial TNF-α overproduction following MI. This finding indicates the essential role of myocardial insulin signaling in protection against ischemic HF.

Genetically determined exercise capacity affects systemic glucose response to insulin in rats

2021 ◽  
Author(s):  
Michael Schwarzer ◽  
Annika Molis ◽  
Christina Schenkl ◽  
Andrea Schrepper ◽  
Steven L. Britton ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Aerobic Exercise ◽  
Exercise Capacity ◽  
Genetic Predisposition ◽  
Citrate Synthase ◽  
Insulin Response ◽  
Glucose Response ◽  
Epididymal Fat ◽  
Aerobic Exercise Capacity ◽  
Genetically Determined

Introduction: Aerobic exercise capacity is inversely related to morbidity and mortality as well as to insulin resistance. However, exercising in patients has led to conflicting results, presumably because aerobic exercise capacity consists of intrinsic (genetically determined) and extrinsic (environmentally determined) parts. The contribution of both parts to insulin sensitivity is also not clear. We investigated sedentary and exercised (aerobic interval training) high (HCR) and low capacity runners (LCR) differing in their genetically determined aerobic exercise capacity to determine the contribution of both parts to insulin sensitivity. Methods and Results: LCR and HCR differed in their untrained exercise capacity and body weight. Sedentary LCR displayed a diabetic phenotype with higher random glucose, lower glucose infusion rate during hyperinsulinemic euglycemic clamping than HCR. Echocardiography showed equal morphological and functional parameters and no change with exercise. Four weeks of exercise caused significant improvements in aerobic exercise capacity, which was more pronounced in LCR. However, with respect to glucose use, exercise affected HCR only. In these animals, exercise increased 2-deoxyglucose uptake in gastrocnemius (+58.5 %, p= 0.1) and in epididymal fat (+106 %; p<0.05). Citrate synthase activity also increased in these tissues (gastrocnemius 69 % epididymal fat 63 %). Conclusion: In our model of HCR and LCR, genetic predisposition for low exercise capacity is associated with impaired insulin sensitivity and impedes exercise-induced improvements in insulin response. Our results suggest that genetic predisposition for low aerobic exercise capacity impairs insulin response, which may not be overcome by exercise.

Sign in / Sign up

Export Citation Format

Share Document