amino acids. The PPARγ1 gene is expressed in nearly all cells, while PPARγ2 expression is limited mainly to adipose tissue [ 2 ]. Both PPARγ1 and PPARγ2 isoforms are an important adipogenic regulator and essential for the control of insulin sensitivity. However, PPARγ2 regulates response to nutrient intake and obesity. These characteristic properties make it a key molecule to be involved in the expression of adipokines such as leptin, adiponectin, resistin and chemerin, which may act as modulators of energy metabolism and insulin action [ 3 ]. Moreover, PPARγ2
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The Secret Life of Fat: What are Fat Cells Doing for the Regulation of Metabolism
Adipose tissue has long been regarded as an organ the sole purpose of which was to store excess energy as triglycerides, and release energy as free fatty acids, which itself is an essential self-defense system for survival during starvation. This point of view has now changed, fat tissue has emerged as an endocrine and secretory organ affecting more than one metabolic pathway. Its major endocrine function is secreting several hormones, notably leptin and adiponectin. Also, adipose tissue releases adipo-kines involved in inflammation and hemostasis: growth factors (TNFα, transforming growth factor-beta, nerve growth factor, VEGF), cytokines (IL-1β, IL-6, IL-10), chemokines (IL-8), acute-phase proteins (haptoglobin, serum amyloid A) and prothrombotic factor (plasminogen activator inhibitor-1). This review aims to present some of the recent topics of selected adipokine research that may be of particular importance.
Background: Hypoadiponectinemia and hyperleptinemia, and reductions in the ratio of adiponectin to leptin (A/L ratio) are associated with the development of hepatic necroinflammation in nonalcoholic fatty liver, but the association of the adipokines with hepatic steatosis in chronic viral hepatitis is unclear.
Objective: To investigate the relationship between serum A/L ratio, insulin resistance, degree of hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis.
Methods: We measured serum adiponectin, leptin, and resistin levels, insulin resistance, and analyzed the association between liver histopathology and the level of the adipokines in 44 patients with chronic viral hepatitis before they started treatment.
Results: We found that insulin resistance, leptin, and resistin levels tended to increase in the group with a greater degree of hepatic steatosis and necroinflammation, but that the increase was not significant. The adiponectin/leptin ratio (A/L ratio) in a group with a low degree of hepatic steatosis was significantly higher than it was in the group with a high degree of hepatic steatosis (3.1 ± 3.1 vs 1.2 ± 0.8; P = 0.008). The A/L ratio in a group with low histological activity index (HAI) scores was significantly higher than in the group with high HAI scores (3.7 ± 3.4 vs 1.1 ± 1.1; P = 0.006). Abdominal obesity was the only variable that showed a significant association with the HAI score (P = 0.03).
Conclusion: The serum A/L ratio in patients with chronic viral hepatitis showed a significant inverse association with their degree of hepatic steatosis and necroinflammation.
et al. Total and highmolecular weight adiponectin in relation to metabolic variables at baseline and in response to an exercise treatment programme. Diabetes Care 30: 280-285, 2007. 32. Luo M, Oza-Frank R, Narayan KMV, Gokulakrishnan K, Mohan V. Serum total adiponectin is associated with impaired glucose tolerance in Asian Indian females but not in males. J Diabetes Sci Technol 4: 645-651, 2010. 33. Tonjes A, Fasshauer M, Kratzsch J, Stumvoll M, Bluher M. Adipokine pattern in subjects with impaired fasting glucose and impaired glucose tolerance in comparison
Relation of Endothelial Dysfunction and Adipokines Levels to Insulin Resistance in Metabolic Syndrome Patients
Obese metabolic syndrome (MS) patients were categorised into three groups: 44 with type 2 diabetes mellitus (T2DM)(D); 20 with T2DM and coronary artery disease (CAD) (DC), and 26 with MS alone (M). Eighteen healthy subjects were selected as controls (C). Insulin resistance (IR) was assessed by HOMA-IR. Adiponectin, tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and interleukin-8 (IL-8) concentrations were measured by xMAP technology. Endothelin-1 (ET-1) was determined by ELISA. We used laser Doppler imaging for evaluating cutaneous endothelium-dependent vasodilatation in the hand. D and DC groups had significantly elevated IR compared with M or C group (P < 0.01). TNF-α, IL-6, IL-8, MCP-1 and ET-1 levels in DC were significantly elevated compared with other groups (P < 0.001). IL-6, IL-8, MCP-1 and ET-1 in D group were higher than those in C group (P < 0.05). TNF-α, IL-6, IL-8, MCP-1 and ET-1 concentrations were correlated with HOMA-IR indexes and adiponectin levels. All patients had lower adiponectin concentrations than controls (P < 0.001), but there were no differences between the patient groups. Only D and DC groups demonstrated a significant and similar decrease in LDI-Ach marker compared to C group (P < 0.001). LDI-Ach values were significantly correlated with HOMA-IR indexes and adiponectin levels (P < 0.001). Our findings show that obese MS patients have significantly increased HOMA-IR, TNF-α, IL-6, MCP-1 and IL-8 levels, decreased adiponectin concentration, and endothelial dysfunction, but the presence of T2DM and CAD in these patients is associated with more pronounced endothelial dysfunction and increased production of inflammatory cytokines and chemokines.