Co-existence of insulin resistance and high concentrations of circulating oxidized LDL lipids.

INTRODUCTION: Insulin metabolism has been previously linked to oxidized low-density lipoproteins (ox-LDL), but corroborating intervention studies are lacking. We investigated whether changes in ox-LDL levels are accompanied by changes in insulin sensitivity in a 32-month life-style intervention study. MATERIALS AND METHODS: A 2-month weight reduction was followed by 6-month diet and exercise counselling and a 2-year follow-up period. Men of 35-50 years of age, BMI ≥ 30 kg/m(2), and waist circumference > 100 cm were recruited via newspapers in the city of Tampere, Finland. Of the 90 men meeting the inclusion criteria, 67 (76%) completed the study. Ox-LDL was estimated as the presence of oxidized lipids in LDL. Homeostasis model assessment of insulin resistance (HOMA-IR), ox-LDL, and ratio of ox-LDL and high-density lipoprotein cholesterol (ox-LDL/HDL-c) were used as the main outcome measures. RESULTS: The detected changes in HOMA-IR were strikingly similar to those in ox-LDL and ox-LDL/HDL-c. Compared to the first HOMA-IR quartile, the fourth quartile had 23%-51% higher concentrations in ox-LDL and ox-LDL/HDL-c at all time points (P < 0.05 for all). CONCLUSION: This weight reduction intervention study adds evidence to support the connection between insulin metabolism and oxidized LDL, possibly contributing to the higher incidence of atherosclerotic cardiovascular diseases among diabetic patients.

Circulating oxidised LDL lipids, when proportioned to HDL-c, emerged as a risk factor of all-cause mortality in a population-based survival study.

BACKGROUND AND OBJECTIVE: the data concerning the predictive role of oxidised LDL (ox-LDL) in all-cause mortality are scarce. We investigated whether circulating ox-LDL would stand out as a risk factor of total mortality in the elderly. Study subjects, design and methods: a total of 1,260 elderly inhabitants (533 men, 727 women) aged 64 years or more from Lieto, South-Western Finland participated the study in 1998-99. Medical records were re-examined approximately a decade later in January 2009. Circulating ox-LDL lipids were used as the main outcome measure. The comparisons were obtained by the Cox hazard ratio model. RESULTS: during the 10-year follow-up, 467 participants had died (37%), of whom 36% had died of atherosclerotic cardiovascular diseases. Ox-LDL was a significant predictor of all-cause mortality, when proportioned to low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c) or apolipoprotein A1 (apoA1). These findings were independent of age, sex, body mass index, smoking, blood pressure and diabetes (P < 0.05 for all). CONCLUSION: circulating ox-LDL lipids, when proportioned to LDL-c, HDL-c or apoaA1, stand out as a risk factor for all-cause mortality independent of major confounding attributes. In the prospective survival and increasing disease burden caused by accumulating age, oxidative stress may have a considerable role.

Smoking and low serum testosterone associates with high concentration of oxidized LDL.

BACKGROUND: The interplay between smoking, oxidized low-density lipoprotein cholesterol (ox-LDL) and gonadal hormones has been scarcely investigated. AIM: To investigate associations in ox-LDL and gonadal hormones in smokers and non-smokers METHODS: Participants (n=164) were obtained from a population cohort of Finnish men aged 40-70 years. The subjects answered a detailed questionnaire on their health behaviour, medication, diseases, and different symptoms, and the hormonal and lipid profiles were measured. RESULTS: Smokers (n=33) had higher levels of ox-LDL (21%) and more free testosterone (12%) (P<0.01 for all) than non-smokers (n=131). The difference between smokers and non-smokers in ox-LDL persisted after controlling for possible confounding factors. When the smokers were divided into two subgroups (n=16 and n=17) according to total testosterone (< or =15 and >15 nmol/L), the ox-LDL in the low-testosterone subgroup was significantly higher (30%) than in the high-testosterone group (P=0.006). Similarly in the corresponding non-smoking subgroups (n=72 and n=59), ox-LDL was significantly higher (11%) in the low-testosterone subgroup than in the high-testosterone subgroup (P=0.012). CONCLUSIONS: Smoking men have significantly more ox-LDL than non-smoking men. Furthermore, if smoking is combined with a low serum testosterone, ox-LDL is even higher. This may suggest a higher risk for atherosclerosis.