scholarly journals Does glucocorticoid exposure explain the association between metabolic dysfunction and tendinopathy?

2020 ◽  
Vol 9 (3) ◽  
pp. R36-R46
Author(s):  
Trevor Lewis ◽  
Eva Zeisig ◽  
Jamie E Gaida
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Tendon Rupture ◽  
Structure And Function ◽  
Metabolic Health ◽  
The Body ◽  
Visceral Adiposity ◽  
And Function ◽  
The Impact

Background While metabolic health is acknowledged to affect connective tissue structure and function, the mechanisms are unclear. Glucocorticoids are present in almost every cell type throughout the body and control key physiological processes such as energy homeostasis, stress response, inflammatory and immune processes, and cardiovascular function. Glucocorticoid excess manifests as visceral adiposity, dyslipidemia, insulin resistance, and type 2 diabetes. As these metabolic states are also associated with tendinopathy and tendon rupture, it may be that glucocorticoids excess is the link between metabolic health and tendinopathy. Objective To synthesise current knowledge linking glucocorticoid exposure to tendon structure and function. Methods Narrative literature review. Results We provide an overview of endogenous glucocorticoid production, regulation, and signalling. Next we review the impact that oral glucocorticoid has on risk of tendon rupture and the effect that injected glucocorticoid has on resolution of symptoms. Then we highlight the clinical and mechanistic overlap between tendinopathy and glucocorticoid excess in the areas of visceral adiposity, dyslipidemia, insulin resistance and type 2 diabetes. In these areas, we highlight the role of glucocorticoids and how these hormones might underpin the connection between metabolic health and tendon dysfunction. Conclusions There are several plausible pathways through which glucocorticoids might mediate the connection between metabolic health and tendinopathy.

scholarly journals Metformin and left ventricular hypertrophy in patients with comorbidity

2017 ◽  
Vol 4 (2) ◽  
pp. 61-64
Author(s):  
Ganna Demydenko
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Essential Hypertension ◽  
Left Ventricle ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Structure And Function ◽  
Metformin Treatment ◽  
And Function

Essential hypertension (EH) stays the important public challenge, because of leading positions in morbidity and mortality in not only Ukraine, but also worldwide. Recent studies have suggested that metformin could inhibit cardiomyocyte apoptosis and improve cardiac function.Aim of the study was to investigate metformin’s influence on left ventricular structure and function in patients with essential hypertension with concomitant type 2 diabetes (T2D).Materials and methods: 120 patients with essential hypertension (EH) were recruited in the study and were divided into three groups according to comorbid state: 60  - EH and T2D; 30 – EH with prediabetes; 30 – EH without dysglicemia. Carbohydrate parameters, left ventricle structure and function were analyzed before and after 12 weeks of metformin treatment.Results. Metformin treatment results in fasting glycaemia and insulin resistance diminishing on 21,79 % and 26,84 %.  Echocardiography in 12 weeks metformin treatment showed significant decreasing of left ventricle myocardium mass for 6,1 %, left ventricle posterior wall thickness - 2,3 %. More pronounced changes in patients with EH and T2D are connected with glucotoxicity, lipotoxicity, insulin resistance diminishing and also with pleiotropic metformin’s effects.Conclusion. Metformin has positive influence to the structure and function of left ventricle with increasing of EDV and LV hypertrophy regress. These findings may provide a potential effectiveness for patients with T2D at risk of developing pathological cardiac hypertrophy.Key words: essential hypertension, type 2 diabetes, left ventricle hypertrophy, metformin.

scholarly journals Visceral Adiposity Index is associated with Insulin Resistance, impaired Insulin Secretion, and β-cell dysfunction in subjects at risk for Type 2 Diabetes

2021 ◽  
pp. 100013
Author(s):  
Froylan David Martínez-Sánchez ◽  
Valerie Paola Vargas-Abonce ◽  
Andrea Rocha-Haro ◽  
Romina Flores-Cardenas ◽  
Milagros Fernández-Barrio ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
At Risk ◽  
Insulin Secretion ◽  
Visceral Adiposity ◽  
Visceral Adiposity Index ◽  
Β Cell ◽  
Cell Dysfunction ◽  
Impaired Insulin

scholarly journals Is visceral adiposity a modifier for the impact of blood pressure on arterial stiffness and albuminuria in patients with type 2 diabetes?

2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Ryotaro Bouchi ◽  
Norihiko Ohara ◽  
Masahiro Asakawa ◽  
Yujiro Nakano ◽  
Takato Takeuchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Arterial Stiffness ◽  
Visceral Adiposity ◽  
The Impact

scholarly journals Effect of Inulin-Type Carbohydrates on Insulin Resistance in Patients with Type 2 Diabetes and Obesity: A Systematic Review and Meta-Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Mingyue Rao ◽  
Chenlin Gao ◽  
Ling Xu ◽  
Lan Jiang ◽  
Jianhua Zhu ◽  
...  
Keyword(s):  
Systematic Review ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Subgroup Analysis ◽  
Meta Analysis ◽  
The Body ◽  
Obese Patients ◽  
Significant Difference ◽  
Simple Obesity

Background. Insulin resistance (IR) is a physiological condition related to type 2 diabetes mellitus (T2DM) and obesity, which is associated with high blood insulin and glucose. Inulin-type carbohydrate (ITC) is a kind of fermentable fructan that can reduce glucose and ameliorate IR in an animal model, but the effect in clinical trials is controversial. Objective. The authors conducted a systematic literature review to evaluate the effect of ITC supplementation in ameliorating IR in T2DM and obese patients. Methods. Multiple databases were queried for studies before December 25, 2018, which involved supplementation with ITC in ameliorating IR in T2DM and obese patients. Studies that involved meta-analysis of the body mass index (BMI), fasting plasma glucose (FPG), fasting insulin (FI), HbA1c, homeostatic model assessment IR (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) of T2DM subjects were included. HOMA-IR and QUICKI were identified as the primary outcomes. A systematic review was performed to evaluate the effect of ITC on IR in obese patients. Results. The database search yielded 25 studies, which met the inclusion criteria; 11 articles were meta-analyzed, and 5 other articles on T2DM and 9 articles on simple obesity were systematically reviewed. Our results did not find ITC supplementation decrease postintervention and reduction data of BMI (P=0.08). However, it can significantly decrease postintervention and reduction data of FPG, FI, HbA1c, and HOMA-IR. Heterogeneity was eliminated by subgroup analysis according to baseline BMI. There was no significant difference in the amelioration of QUICKI between the ITC and control groups. However, the difference was statistically significant and the heterogeneity was eliminated after subgroup analysis according to intakes of ITC. 14 articles for a systematic review found that the results of blood glucose, insulin, and HbA1c were controversial. Only one of the seven studies on simple obesity concluded that ITC intervention significantly ameliorated HOMA-IR, while the other six did not. Conclusion. Supplementation of ITC can ameliorate IR in T2DM, especially in obese T2DM patients, but the effects are controversial in obese patients.

scholarly journals Ethnic distinctions in the pathophysiology of type 2 diabetes: a focus on black African-Caribbean populations

2019 ◽  
Vol 79 (2) ◽  
pp. 184-193 ◽  
Author(s):  
Louise M. Goff ◽  
Meera Ladwa ◽  
Olah Hakim ◽  
Oluwatoyosi Bello
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Global Public Health ◽  
Black African ◽  
African Caribbean ◽  
Black Populations ◽  
The Impact ◽  
Caribbean Populations

Type 2 diabetes (T2D) is a global public health priority, particularly for populations of black African-Caribbean ethnicity, who suffer disproportionately high rates of the disease. While the mechanisms underlying the development of T2D are well documented, there is growing evidence describing distinctions among black African-Caribbean populations. In the present paper, we review the evidence describing the impact of black African-Caribbean ethnicity on T2D pathophysiology. Ethnic differences were first recognised through evidence that metabolic syndrome diagnostic criteria fail to detect T2D risk in black populations due to less central obesity and dyslipidaemia. Subsequently more detailed investigations have recognised other mechanistic differences, particularly lower visceral and hepatic fat accumulation and a distinctly hyperinsulinaemic response to glucose stimulation. While epidemiological studies have reported exaggerated insulin resistance in black populations, more detailed and direct measures of insulin sensitivity have provided evidence that insulin sensitivity is not markedly different to other ethnic groups and does not explain the hyperinsulinaemia that is exhibited. These findings lead us to hypothesise that ectopic fat does not play a pivotal role in driving insulin resistance in black populations. Furthermore, we hypothesise that hyperinsulinaemia is driven by lower rates of hepatic insulin clearance rather than heightened insulin resistance and is a primary defect rather than occurring in compensation for insulin resistance. These hypotheses are being investigated in our ongoing South London Diabetes and Ethnicity Phenotyping study, which will enable a more detailed understanding of ethnic distinctions in the pathophysiology of T2D between men of black African and white European ethnicity.

scholarly journals Insulin Resistance in Osteoarthritis: Similar Mechanisms to Type 2 Diabetes Mellitus

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Elena V Tchetina ◽  
Galina A Markova ◽  
Eugeniya P Sharapova
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
The Body ◽  
Whole Body ◽  
Insulin Resistant ◽  
Resistant State ◽  
Insulin Resistant State

Osteoarthritis (OA) and type 2 diabetes mellitus (T2D) are two of the most widespread chronic diseases. OA and T2D have common epidemiologic traits, are considered heterogenic multifactorial pathologies that develop through the interaction of genetic and environmental factors, and have common risk factors. In addition, both of these diseases often manifest in a single patient. Despite differences in clinical manifestations, both diseases are characterized by disturbances in cellular metabolism and by an insulin-resistant state primarily associated with the production and utilization of energy. However, currently, the primary cause of OA development and progression is not clear. In addition, although OA is manifested as a joint disease, evidence has accumulated that it affects the whole body. As pathological insulin resistance is viewed as a driving force of T2D development, now, we present evidence that the molecular and cellular metabolic disturbances associated with OA are linked to an insulin-resistant state similar to T2D. Moreover, the alterations in cellular energy requirements associated with insulin resistance could affect many metabolic changes in the body that eventually result in pathology and could serve as a unified mechanism that also functions in many metabolic diseases. However, these issues have not been comprehensively described. Therefore, here, we discuss the basic molecular mechanisms underlying the pathological processes associated with the development of insulin resistance; the major inducers, regulators, and metabolic consequences of insulin resistance; and instruments for controlling insulin resistance as a new approach to therapy.

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