Inflammation of adipose tissue. Part 2. Pathogenetic role in type 2 diabetes mellitus

This review deals with the role of adipose tissue inflammation (ATI) in the development of type 2 diabetes mellitus (DM2). ATI is regarded as a link between obesity and DM2. The review illustrates the involvement of main adipokines in pathogenesis of DM2 and provides a detailed description of such factors as impaired adiponectin and stimulation of cytokine production responsible for metabolic disorders, activation of lipolysis, in adipocytes, increased fatty acid and triglyceride levels, suppression of insulin activity at the receptor and intracellular levels. Adipokines, in the first place cytokines, act on the insulin signal pathway and affect the intracellular inflammatory kinase cascade. At the intercellular level, ATI stimulates JNK and IKK-beta/kB responsible for the development of insulin resistance via such mechanisms as activation of cytokine secretion in the adipose tissue, oxidative stress, and induction of endoplasmic reticulum enzymes. The key role of JNK and IKK-beta/kB in the inhibition of the insulin signal pathway is mediated through inactivation of insulin receptor substrate 1. Also, it is shown that ATI modulates B-cell function and promotes progressive reduction of insulin secretion.

Download Full-text

The role of nonesterified fatty acids in pathogenesis of cardiovascular diseases

Arterial’naya Gipertenziya (Arterial Hypertension) ◽

10.18705/1607-419x-2010-16-1-93-103 ◽

2010 ◽

Vol 16 (1) ◽

pp. 93-103 ◽

Cited By ~ 2

Author(s):

M. V. Tsvetkova ◽

V. N. Khirmanov ◽

N. N. Zybina

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Fatty Acids ◽

Type 2 Diabetes Mellitus ◽

Adipose Tissue ◽

Risk Factor ◽

Cardiovascular Diseases ◽

Sudden Death

The paper reviews publications concerned the role of nonesterifi ed fatty acids (NEFA) in pathogenesis of cardiovascular diseases. NEFAs are four and more carbons chain length carbonic acids and they are presented in free form (nonesterifi ed) in human body. Plasma NEFAs are produced by the adipose tissue triglyceride lipolysis, another source are lipoproteins such as chylomicrons, very low density lipoproteins and intermediate density lipoproteins. Elevated NEFA concentrations in plasma are the risk factor of cardiovascular diseases and type 2 diabetes mellitus and the independent risk factor of hypertension and sudden death. NEFA plasma concentration is elevated in atherosclerosis, acute myocardial infarction, diabetes mellitus, obesity, hypertension, and often in metabolic syndrome. A probable cause of NEFAs accumulation in plasma may be overeating and low physical activity, which result in increase of adipose tissue mass, lipolysis intensifi cation and elevation of NEFAs concentration in plasma. The role of elevated plasma NEFA concentration in a number of conditions (abdominal obesity, atherogenic dyslipidemia, insulin resistance, type 2 diabetes mellitus, endothelial dysfunction, vascular infl ammation, atherosclerosis, hypertension, ischemic heart disease, rhythm disturbances, sudden death) and possible ways of their correction are discussed.

Download Full-text

Important role of fat tissue hormones in development of comorbid chronic pancreatitis and obesity

Herald of Pancreatic Club ◽

10.33149/vkp.2017.03.03 ◽

2017 ◽

Vol 37 (3) ◽

pp. 30-35

Author(s):

T. N. Hristich

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Adipose Tissue ◽

Chronic Pancreatitis ◽

Pancreatic Disease ◽

Pancreatic Tissue ◽

Visceral Adipose

Aim of this paper is to consider the role of hormones of the adipose tissue in mechanisms of obesity, metabolic syndrome, type 2 diabetes mellitus upon chronic pancreatitis. Materials and methods. The literature review indicates the value of visceral fat in the development of insulin resistance, dyslipidemia, including atherogenic one, taking into account the possible infiltration of pancreatic tissue by adipocytes. Participation of some adipocytokines of adipose tissue in the development of obesity upon chronic pancreatitis is highlighted. It is shown that in some cases the hormones of visceral adipose tissue, penetrating through the portal vein to the liver and then to the pancreas, aggravated the course of systemic chronic inflammation of the inherent chronic pancreatitis, promote steatosis and development of fatty pancreatic disease. Conclusion. Literary sources indicate the leading role of visceral adipose tissue and its hormones in the formation of obesity in chronic pancreatitis. Due to the infiltration of the pancreatic tissue by adipocytes, lipoidosis and steatosis develop. With the progression of the process type 2 diabetes mellitus, fatty liver or pancreatic disease, or cancer of these orhans. Consequently, there is a need for serious differentiated preventive and curative measures aimed at promoting a healthy lifestyle to improve the quality of life of patients suffering from chronic pancreatitis.

Download Full-text

The role of adipose tissue M1/M2 macrophages in type 2 diabetes mellitus

Diabetology International ◽

10.1007/s13340-020-00482-2 ◽

2020 ◽

Vol 12 (1) ◽

pp. 74-79

Author(s):

Shiho Fujisaka

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Adipose Tissue ◽

M2 Macrophages

Download Full-text

Serum Cytokine Dependent Hematopoietic Cell Linker (CLNK) as a Predictor for the Duration of Illness in Type 2 Diabetes Mellitus

10.20944/preprints202004.0463.v1 ◽

2020 ◽

Author(s):

Suhaer Zeki Al-Fadhel ◽

Nibras H. Abdulsada Al-Ghuraibawi ◽

Dunia M. Mohammed Ali ◽

Hussein Kadhem Al-Hakeim

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Cell Function ◽

Adaptor Protein ◽

Correlation Study ◽

Hematopoietic Cell ◽

Receptor Signaling

Type 2 diabetes mellitus (T2DM) is an endocrine illness associate with various changes in the immune system and adaptor protein levels. Cytokine dependent hematopoietic cell linker (CLNK) is an adapter protein that regulates immune receptor signaling and acts as a regulator of the receptor signaling of T-cells and natural killer T-cell. The role of CLNK in T2DM is not studied previously. In the present study, serum CLNK level was measured and correlated with some sociodemographic and insulin resistance (IR) parameters. This is achieved by performing measurement of CLNK and insulin parameters (glucose, insulin, and HbA1c in addition to the calculation of the functions of IR (HOMA2IR), insulin sensitivity (HOMA%S), and beta-cell function (HOMA%B)) in 60 T2DM patients and 30 controls. The results indicated a significant increase (p=0.025) in serum CLNK in patients group in comparison with the controls. Multivariate generalized linear model (GLM) analysis revealed no significant effect of age, BMI, and sex on the CLNK level. The results of tests for between-subjects showed that the CLNK affects diagnosis significantly (F=7.445, p=0.008, partial η2 =0.081) and its effect is approximately the same as the effect of insulin (F=8.107, p=0.006, partial η2 =0.087). The correlation study showed a highly significant positive correlation between CLNK and the duration of disease (rho=0.420, p<0.001). It can be concluded that the increase CLNK in T2DM revealing the role of the adaptor proteins level in the nature of disease. Elevation of CLNK level may be used as a predictor for diabetes complications, which needs more investigations.

Download Full-text