Age-associated decline of monocyte insulin sensitivity in diabetic and healthy individuals

Nakamura, Suguru; Mori, Kentaro; Okuma, Hideyuki; Sekine, Tetsuo; Miyazaki, Asako; Tsuchiya, Kyoichiro

doi:10.1177/1479164121989281

Cited by 7 publications

(4 citation statements)

References 33 publications

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“…Нарушения углеводного обмена являются факторами, связанными со старением сосудов и приводящими к риску ССЗ. C возрастом растут средние уровни гликемии и снижается чувствительность тканей к инсулину, что независимо от наличия СД-2 приводит к ССЗ [12]. ИР отражает не толь-ко хронически существующую гипергликемию, но также дислипидемию и метаболические нарушения.…”

Section: Discussionunclassified

Biological vascular age and its relationship with cardiovascular risk factors

Akopyan

Strazhesko

Klyashtorny

et al. 2022

Cardiovasc Ther Prev

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Aim. To study of the relationship between cardiovascular risk factors and biological vascular age.Material and methods. The biological vascular age was estimated using models based on the arterial wall parameters. Using multiple logistic and linear regression, we studied the relationship between the biological vascular age and cardiovascular risk factors in 143 people without cardiovascular disease (CVD). Persons with a positive difference between the vascular and chronological age were assigned to the “old” vascular group, and persons with no or negative difference between the vascular and chronological age were assigned to the “young” vascular group.Results. Linear regression in the “young” vascular group showed an inverse relationship between the difference between the vascular and chronological age with the levels of low-density lipoprotein cholesterol (p=0,001; β±SE=-1,67±0,47), triglycerides (p=0,017; β±SE=-1,66±0,68), urea (p=0,025; β±SE=-0,89±0,39) and insulin resistance index (p=0,001; β±SE=-1,22±0,36). In the “old” vascular group, a direct relationship was found between the difference between the vascular and chronological age and central systolic blood pressure (p=0,015; β±SE=0,10±0,04). According to logistic regression, the likelihood of having “old” vessels increased by 1,23 times with an increase in blood glucose levels by 0,5 mmol/l (p=0,044; odds ratio (OR)=1,23; 95% confidence interval (CI): 1,011,51), the presence of hypertension (p=0,034; OR=3,11; 95% CI: 1,09-8,86) and type 2 diabetes (p=0,025; OR=3,61; 95% CI: 1,1711,09), as well as decreased by 2 times with an increase in high-density lipoprotein cholesterol by 0,3 mmol/l (p=0,003; OR=0,5; 95% CI: 0,32-0,79).Conclusion. The difference between the biological vascular age and chronological age is associated with traditional CVD risk factors.

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Section: Discussionunclassified

Biological vascular age and its relationship with cardiovascular risk factors

Akopyan

Strazhesko

Klyashtorny

et al. 2022

Cardiovasc Ther Prev

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“…Levels of the IR mRNA in these different vascular beds are decreased in AD ( Figure 2 D). However, it should be noted the IR mRNA values reported have been quite variable [ 46 ]. Therefore, follow up studies measuring protein levels are needed to fully assess the expression levels present in tissues, cell types, and even cerebrovascular beds.…”

Section: Insulin Receptor and Signalingmentioning

confidence: 99%

“…Insulin resistance has even been detected in isolated cultured human monocytes. Not only are IR mRNA levels decreased with type 2 diabetes compared to those controls without a history of type 2 diabetes, but the insulin-stimulated IR signaling response is also blunted in those individuals with type 2 diabetes [ 46 ]. This study also shows that insulin resistance, as measured by the insulin-stimulated Akt phosphorylation response, correlates with age in both the control group and the type 2 diabetes group.…”

Section: Peripheral Insulin Resistancementioning

confidence: 99%

Insulin Resistance in Peripheral Tissues and the Brain: A Tale of Two Sites

2022

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The concept of insulin resistance has been around since a few decades after the discovery of insulin itself. To allude to the classic Charles Dicken’s novel published 62 years before the discovery of insulin, in some ways, this is the best of times, as the concept of insulin resistance has expanded to include the brain, with the realization that insulin has a life beyond the regulation of glucose. In other ways, it is the worst of times as insulin resistance is implicated in devastating diseases, including diabetes mellitus, obesity, and Alzheimer’s disease (AD) that affect the brain. Peripheral insulin resistance affects nearly a quarter of the United States population in adults over age 20. More recently, it has been implicated in AD, with the degree of brain insulin resistance correlating with cognitive decline. This has led to the investigation of brain or central nervous system (CNS) insulin resistance and the question of the relation between CNS and peripheral insulin resistance. While both may involve dysregulated insulin signaling, the two conditions are not identical and not always interlinked. In this review, we compare and contrast the similarities and differences between peripheral and CNS insulin resistance. We also discuss how an apolipoprotein involved in insulin signaling and related to AD, apolipoprotein E (apoE), has distinct pools in the periphery and CNS and can indirectly affect each system. As these systems are both separated but also linked via the blood–brain barrier (BBB), we discuss the role of the BBB in mediating some of the connections between insulin resistance in the brain and in the peripheral tissues.

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“…In addition, the phenotype of their precursors, monocytes, is modified in obese and diabetic patients [ 80 ]. A higher pro-inflammatory profile is associated with monocyte insulin resistance which is enhanced by ageing in a diabetes-independent manner [ 81 ].…”

Section: Physiopathological Mechanismsmentioning

confidence: 99%

Diabesity in Elderly Cardiovascular Disease Patients: Mechanisms and Regulators

Garcia‐Vega¹,

González-Juanatey

Eiras

2022

IJMS

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Cardiovascular disease (CVD) is the leading cause of death in the world. In 2019, 550 million people were suffering from CVD and 18 million of them died as a result. Most of them had associated risk factors such as high fasting glucose, which caused 134 million deaths, and obesity, which accounted for 5.02 million deaths. Diabesity, a combination of type 2 diabetes and obesity, contributes to cardiac, metabolic, inflammation and neurohumoral changes that determine cardiac dysfunction (diabesity-related cardiomyopathy). Epicardial adipose tissue (EAT) is distributed around the myocardium, promoting myocardial inflammation and fibrosis, and is associated with an increased risk of heart failure, particularly with preserved systolic function, atrial fibrillation and coronary atherosclerosis. In fact, several hypoglycaemic drugs have demonstrated a volume reduction of EAT and effects on its metabolic and inflammation profile. However, it is necessary to improve knowledge of the diabesity pathophysiologic mechanisms involved in the development and progression of cardiovascular diseases for comprehensive patient management including drugs to optimize glucometabolic control. This review presents the mechanisms of diabesity associated with cardiovascular disease and their therapeutic implications.

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Age-associated decline of monocyte insulin sensitivity in diabetic and healthy individuals

Cited by 7 publications

References 33 publications

Biological vascular age and its relationship with cardiovascular risk factors

Biological vascular age and its relationship with cardiovascular risk factors

Insulin Resistance in Peripheral Tissues and the Brain: A Tale of Two Sites

Diabesity in Elderly Cardiovascular Disease Patients: Mechanisms and Regulators

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