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The present review aimed to present the research highlights on C1q/TNF-related protein 1 (CTRP1), a member of the recently discovered family of highly conserved adiponectin paralog proteins, C1q tumor necrosis factor-related proteins. CTRP1 plays an important role in regulating body energy homeostasis and sensitivity to insulin. Studies on animal models have shown that it lowers the concentration of glucose. Elevated concentrations of CTRP1 reduce weight gain and diet-induced insulin resistance. CTRP1 limits the extent of ischemia-reperfusion injury in acute myocardial infarction. It inhibits platelet aggregation by blocking von Willebrand factor binding to collagen. In patients with chronic kidney disease, an increase in CTRP1 levels is associated with a lesser degree of disease progression. CTRP1 stimulates aldosterone synthesis in the adrenal cortex by affecting aldosterone synthase expression. In dehydration, an increase in CTRP1 concentration helps to maintain normotension. It participates in processes related to the proliferation and maturation of chondrocytes. It also promotes atherosclerosis, and a surge in its concentration is correlated with a higher cardiovascular risk in patients with coronary atherosclerosis. In vascular smooth muscle cells, it induces the expression of proinflammatory cytokines. An increase in CTRP1 levels is correlated with the progression of the neoplastic process in patients with glioblastoma.

Reduced postprandial secretion of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), cholecystokinin, and increased hunger was reported after a single dose of orlistat, an inhibitor of intestinal lipase. As yet, the influence of long-term therapy with orlistat on PYYand GLP-1 release has not been studied. Our study was aimed at assessing the influence of 8-week therapy with orlistat as a component of a weight loss program on pre-prandial circulating PYY and GLP-1 levels.

Background: Reduced postprandial secretion of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), cholecystokinin, and increased hunger was reported after a single dose of orlistat, an inhibitor of intestinal lipase. As yet, the influence of long-term therapy with orlistat on PYY and GLP-1 release has not been studied. Our study was aimed at assessing the influence of 8-week therapy with orlistat as a component of a weight loss program on pre-prandial circulating PYY and GLP-1 levels. Methods: Forty obese women, without concomitant diseases, were randomly allocated to groups receiving orlistat or placebo during an 8-week weight management program. Body mass, body composition and plasma levels of PYY, GLP-1 and insulin (for QUICKI calculation) were determined prior to and at the end of therapy. Results: Women treated with orlistat obtained significantly greater body and fat mass loss than those receiving placebo (9.0 ± 3.1 vs. 5.9 ± 3.2% and 21.9 ±10.9 vs. 7.4 ± 15.6%, respectively). Only in those treated with orlistat a slight, but significant increase of the QUICKI was found (8.0 ± 16.5 vs. -0.1 ± 12.7%, respectively). Weight loss was followed by a significant increase of plasma levels of PYY and GLP-1 in group treated with orlistat, and was about 2-times greater than receiving placebo. The increase was independent of body mass changes. Conclusion: The long-term inhibition of intestinal lipase by orlistat increases the pre-prandial levels of GLP-1 and PYY, independent of body mass changes. Therefore, it seems that long-term treatment with orlistat may exert hunger suppressing and insulin sensitizing incretin effect beyond weight reduction.

Objective— The inflammatory processes as well as the lipid disturbances play an important role in the pathogenesis of atherosclerosis.The aim of the study was to evaluate the influence of the hyperlipidaemias on serum levels of tumour necrosis factor (TNF) α, the soluble form of TNF receptor (sTNFR) 1 and 2, Interleukin (IL)-10 in patients with stable coronary artery disease (CAD).Methods and results— The study group comprised 94 consecutive admissions with stable CAD: 39 patients with hypercholesterolaemia (group HC), 22 patients with mixed hyperlipidaemia (group HL) and 33 patients with normal lipids (group NL).Twenty healthy volunteers were the controls (group C).Serum TNFα levels were higher in all CAD groups (p<0.001) than in healthy subjects. Mean serum concentrations of sTNFR 1 were significantly higher in group NL (p<0.05) in comparison both to group HC and controls. IL-10 levels were higher in group HC than in controls (p<0.05).In all CAD patients TNFα showed a negative correlation with HDL-cholesterol (p<0.001) and a positive correlation with triglycerides (p<0.001). Moreover, sTNFR 1 and IL-10 showed a negative (p<0.05) and sTNFR 2 a positive correlation with LDL-cholesterol (p<0.001).Conclusions— CAD patients are characterized by increased serum concentrations of TNFα. It seems likely that immune activation (TNFα, sTNFR 1, sTNFR 2, and IL-10) in CAD patients is related to serum lipids levels.