Serum complement and familial combined hyperlipidemia

Ylitalo, Kati; Porkka, Kimmo; Meri, Seppo; Nuotio, Ilpo; Suurinkeroinen, Leena; Vakkilainen, Juha; Pajukanta, Päivi; Viikari, Jorma; Peltonen, Leena; Ehnholm, Christian; Taskinen, Marja‐Riitta

doi:10.1016/s0021-9150(96)06054-6

Cited by 28 publications

(30 citation statements)

References 24 publications

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“…6 There is a correlation between C3 and the majority of conventional risk factors, both in the general population 4 as well as in patients with cardiovascular disease. 5 Increases in C3 were observed in patients with type 2 diabetes, 21,22 hypertension 22 and dyslipidemia, 27 even in the absence of obesity. Our study revealed an additive effect of these diseases on C3.…”

Section: Discussionmentioning

confidence: 99%

Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors

et al. 2007

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Objective: Increased C3 has been related to body mass index (BMI) and insulin resistance, although there are not sufficient studies in subjects with morbid obesity. The purpose of this study was to evaluate the levels of C3 as a function of the BMI in subjects of both sexes, with severe, morbid and extreme obesity, and their possible relationship to insulin resistance or associated diseases such as diabetes, hypertension and dyslipidemia. Subjects: The study included a total of 316 patients (110 men and 206 women) with severe obesity (17.1%), morbid obesity (54.4%) and extreme obesity (28.4%), with an average BMI of 46.7077.37 kg/m 2 . Measurements: The glucose and insulin levels were determined baseline, and 2 h after a 75 g of oral glucose load. The homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated. A lipid profile (total cholesterol, triglycerides, high-density lipoprotein cholesterol, apolipoprotein AI and apolipoprotein B100) was obtained and C3 levels determined by nephelometry. Results: When distributing the patients by quartiles of BMI, we found a progressive increase in the levels of C3, and no significant differences in the rest of analytical variables studied were found; the mean values of C3 were 127.78729.7 mg/dl. A significant correlation was found between C3 and the BMI (r ¼ 0.263, Po0.001), baseline insulin (r ¼ 0.237, P ¼ 0.001) and HOMA-IR (r ¼ 0.237, P ¼ 0.001). High blood pressure was found in 111 patients, type 2 diabetes in 74 patients and dyslipidemia in 139 cases. When distributing the levels of C3 according to the number of associated risk factors (hypertension, diabetes and dyslipidemia), we found significant differences between these patients and those who presented no associated diseases (Po0.01). Conclusion: A relationship between C3 and the progressive increase of BMI in subjects with severe, morbid or extreme obesity was established. This increase in C3 was closely related to insulin levels and the values for HOMA-IR. Furthermore, we also found an increase in C3 as more diseases related to insulin resistance, such as diabetes, hypertension and dyslipidemia, were associated with the obesity.

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Section: Discussionmentioning

confidence: 99%

Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors

et al. 2007

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“…Elevated C3 concentration levels have been reported in individuals with obesity, 51 type 2 diabetes, 52 hypertension, 53 dyslipidemia, 25 and coronary artery disease, 54 all of Pearson's coefficients (R) were calculated for all data and the four groups individually. Non-normally distributed parameters were log-transformed prior to analysis.…”

Section: Discussionmentioning

confidence: 99%

“…China), with ranges comparable to published control values for this assay (range 0.75-3.66 g/l) in a similar adult population. 25,26 Plasma ASP concentration (10.3-58.1 nmol/l) was measured via a sandwich ELISA immunoassay as previously described in detail. 27,28 Calculations and statistical analyses Body mass index (BMI) was measured as weight (kg) per height (m 2 ).…”

Section: Analytical Proceduresmentioning

confidence: 99%

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

et al. 2005

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Objective: The purpose of this study was to determine the relationships between adipocyte hormones acylation stimulating protein (ASP), adiponectin, complement C3 (C3) (ASP precursor) and insulin, C-reactive protein (CRP), lipid profiles and insulin resistance in lean vs obese type 2 diabetes subjects. Subjects: Lean type 2 diabetes subjects (DL n ¼ 27) vs obese type 2 diabetes subjects (DO n ¼ 55) were compared to agematched nondiabetic groups (Obese, OB n ¼ 55 and control, CTL n ¼ 50).Results: The DO group demonstrated significant increases in plasma ASP and C3 with decreases in plasma adiponectin as compared to CTL. Interestingly, these increases in ASP and C3 were as high, or greater, in the DL group in spite of normal weight. By contrast adiponectin in the DL group was comparable to CTL, in spite of marked insulin resistance. C3 correlated with insulin, glucose and homeostasis model assessment of insulin resistance (HOMA-IR); ASP correlated with body mass index (BMI), glucose, insulin and plasma lipid parameters (non-esterified fatty acids (NEFA), triglyceride, cholesterol and apolipoprotein B). Adiponectin correlated with BMI, glucose, NEFA, triglyceride, high-density lipoprotein cholesterol and apolipoprotein A1 but not HOMA-IR, ASP or C3. CRP correlated only with HOMA-IR. Conclusion: Increased ASP and C3 are both associated with diabetes and related lipid factors but are not regulated coordinately. Adiponectin appears to be more closely related to body size (decreased in obese subjects) than insulin resistance in these subjects.

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“…Previous work makes it clear that C3 is significantly elevated in patients with conditions such as obesity, type II diabetes and dyslipidaemia. Fasting C3 concentrations are significantly raised in Pima Indians, 7 and in familial combined hyperlipidemia (FCHL), 15 while C3 mRNA is raised in the subcutaneous fat of obese subjects. 16 It has been proposed that increased levels of C3 and other inflammatory markers in diabetes result from chronic inflammation induced by 'excess' fat tissue.…”

Section: Discussionmentioning

confidence: 99%

Response of the alternative complement pathway to an oral fat load in first-degree relatives of subjects with type II diabetes

et al. 2004

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OBJECTIVE:To investigate levels of components of the alternative pathway of complement, and of two activation products, ASP and Bb, in persons ranging in insulin resistance both fasting and following the consumption of a high-fat, low-carbohydrate meal. SUBJECTS: Healthy controls (n ¼ 17) and normoglycaemic first-degree relatives of patients with type II diabetes (n ¼ 15). MEASUREMENTS: All subjects had normal glucose tolerance. Blood was collected for the measurement of plasma glucose, insulin, triglycerides and free fatty acids. Body composition was assessed with dual energy X-ray absorptiometry (DEXA) and whole-body insulin sensitivity with a euglycaemic, hyperinsulinaemic clamp. Basal and postprandial values over 6 h were determined for plasma C3, B, D, Bb and ASP. Basal levels of C1q, C4 and CRP were also determined. RESULTS: Controls did not differ significantly from the relatives of patients with type II diabetes for any metabolic parameter except in their degree of insulin resistance and central fat (kg). Across all subjects, basal levels of C3, but no other complement protein, were correlated with insulin resistance. Native complement proteins, but not ASP or Bb, were correlated with body mass index and the amount (kg) of central fat. Basal levels of C3 and factor B were significantly higher in the relatives group, whereas factor D and the classical pathway proteins C1q and C4 did not differ between the two groups. Postprandially, levels of factor D were significantly reduced in both groups. ASP levels also fell postprandially, the decline achieving significance in the relatives group. CONCLUSIONS: Elevated levels of C3 and factor B in the diabetic relatives group may have resulted from increased synthesis by adipose tissue. There was no evidence of alternative pathway activation in response to a fat meal in terms of ASP or Bb production, or significant consumption of C3 and factor B. These data do not support an essential requirement of the hypothesis that ASP is produced in response to the intake of fat.

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Serum complement and familial combined hyperlipidemia

Cited by 28 publications

References 24 publications

Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors

Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

Response of the alternative complement pathway to an oral fat load in first-degree relatives of subjects with type II diabetes

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