“…Taken together, our results seem to raise the possibility that a diet treatment reduces PON-1. Whether the mechanism was due to metabolic changes of HDL-C [14, 18] or a reaction to diet- and weight loss-induced reduction of oxidation (as described later) remains to be determined presently, but at least, our study adds to the present knowledge in two main areas: 1) the results from a better defined cohort of a homogeneous population of healthy and overweight/obese (non-morbidly) individuals and a well-controlled intervention by diet alone, 2) the novelty of demonstrating a decrease in lactonase activity that parallels the mono-esterase and tri-esterase changes.…”
Section: Discussionmentioning
confidence: 99%
“…The clinical significance and detailed mechanism of this is presently unclear, so accumulating data are required. Turnover studies have documented the changes in clearance of HDL-C during dietary modification [18], and the reduction in chylomicron-derived HDL formation following caloric (lipid) restriction diet is discussed as an alternate explanation [14]. There is an opinion that the diet-induced HDL-C drop does not increase CVD risk [19]; however, whether this diet-induced reduction of HDL-C is beneficial/harmful remains debatable.…”
Low caloric diet (LCD) is used for weight loss. Paraoxonase 1 (PON-1) is associated with the antioxidant functions of high-density lipoprotein (HDL). Among limited data on the relationships between obesity and PON-1, there has been no study on the effects of a stand-alone LCD on the physiological lactonase activity of PON-1. We investigated the prospective effects of LCD intervention (2 months) for weight loss on serum PON-1 activities (lactonase, arylesterase [mono-esterase] and tri-esterase) and HDL cholesterol (HDL-C), and their association with low-density lipoprotein cholesterol (LDL-C) in overweight and non-morbidly obese but otherwise healthy women (n = 30; mean age, 50.3 years; mean body mass index [BMI], 28.5 kg/m2). In addition to the data such as BMI, blood pressure, blood glucose and lipids, PON-1 activities were examined between pre- and post-intervention. The intervention reduced all metabolic outcomes, and PON-1 lactonase activity (determined with 5-[thiobutyl]butyrolactone) significantly decreased by 6.1%, paralleled by arylesterase (by 7.3%) and tri-esterase (by 7.8%). In multiple regression analysis, the percent change of PON-1 lactonase was significantly, positively and independently correlated to that of LDL-C (β = 0.51), HDL-C (β = 0.40), and BMI (β = 0.37). Our results showed that the solo diet treatment on weight loss might reduce serum PON-1 lactonase activity with reduced HDL-C and LDL-C. The relationship between the lactonase and LDL-C may be adaptive, plausibly hypothesizing less need for PON-1 activity as an antioxidant property to protect lipoproteins. Further research is needed to confirm this prediction.
“…Taken together, our results seem to raise the possibility that a diet treatment reduces PON-1. Whether the mechanism was due to metabolic changes of HDL-C [14, 18] or a reaction to diet- and weight loss-induced reduction of oxidation (as described later) remains to be determined presently, but at least, our study adds to the present knowledge in two main areas: 1) the results from a better defined cohort of a homogeneous population of healthy and overweight/obese (non-morbidly) individuals and a well-controlled intervention by diet alone, 2) the novelty of demonstrating a decrease in lactonase activity that parallels the mono-esterase and tri-esterase changes.…”
Section: Discussionmentioning
confidence: 99%
“…The clinical significance and detailed mechanism of this is presently unclear, so accumulating data are required. Turnover studies have documented the changes in clearance of HDL-C during dietary modification [18], and the reduction in chylomicron-derived HDL formation following caloric (lipid) restriction diet is discussed as an alternate explanation [14]. There is an opinion that the diet-induced HDL-C drop does not increase CVD risk [19]; however, whether this diet-induced reduction of HDL-C is beneficial/harmful remains debatable.…”
Low caloric diet (LCD) is used for weight loss. Paraoxonase 1 (PON-1) is associated with the antioxidant functions of high-density lipoprotein (HDL). Among limited data on the relationships between obesity and PON-1, there has been no study on the effects of a stand-alone LCD on the physiological lactonase activity of PON-1. We investigated the prospective effects of LCD intervention (2 months) for weight loss on serum PON-1 activities (lactonase, arylesterase [mono-esterase] and tri-esterase) and HDL cholesterol (HDL-C), and their association with low-density lipoprotein cholesterol (LDL-C) in overweight and non-morbidly obese but otherwise healthy women (n = 30; mean age, 50.3 years; mean body mass index [BMI], 28.5 kg/m2). In addition to the data such as BMI, blood pressure, blood glucose and lipids, PON-1 activities were examined between pre- and post-intervention. The intervention reduced all metabolic outcomes, and PON-1 lactonase activity (determined with 5-[thiobutyl]butyrolactone) significantly decreased by 6.1%, paralleled by arylesterase (by 7.3%) and tri-esterase (by 7.8%). In multiple regression analysis, the percent change of PON-1 lactonase was significantly, positively and independently correlated to that of LDL-C (β = 0.51), HDL-C (β = 0.40), and BMI (β = 0.37). Our results showed that the solo diet treatment on weight loss might reduce serum PON-1 lactonase activity with reduced HDL-C and LDL-C. The relationship between the lactonase and LDL-C may be adaptive, plausibly hypothesizing less need for PON-1 activity as an antioxidant property to protect lipoproteins. Further research is needed to confirm this prediction.
“…The low HDL observed in obesity is associated with an enhanced risk of atherogenesis possibly due to increased degradation and/or decreased production of HDL particles. Adipose cells have been shown to bind to HDL [7], hence increased body fat may lead to an increased uptake of HDL particles from circulation resulting in a reduction in plasma HDL levels [8]. On the other hand, an increase in HDL has been associated with decreased risk of coronary artery disease [9], probably due to its role in the reverse cholesterol transport process where cholesterol in peripheral tissues is transported to the liver for reuse or bile acid synthesis, preventing the accumulation of cholesterol in the arteries [10].…”
Section: Importance Of Hdlmentioning
confidence: 99%
“…Only three studies reported weight loss after the first phase of VLCD [8, 21, 31] and all three studies report a significant weight loss. Weight loss at the end of the study was significant for all five studies.…”
Section: Effect Of Intermittent Use Of Vlcd On Hdl Levelsmentioning
This paper investigates the effects of very-low-calorie diets (VLCDs) used in the treatment of obesity on high-density lipoprotein (HDL) levels. Although the studies varied widely in their intervention format, duration, and baseline HDL levels, it would appear that HDL levels usually decrease during active weight loss using a VLCD, but these either return to pre-VLCD levels or improve overall during the weight-maintenance phase. More research needs to be done to determine optimal weight-maintenance programmes and the effects of VLCDs in the short term as well as on HDL levels in groups at increased risk of coronary heart disease.
“…This study estimated that, with every kilogram of body weight loss, the concentration of HDL decreases by 0.27 mg/dl, but when the subject’s weight is stabilized, it increases by 0.35 mg/dl per kilogram of weight loss [25]. The responsible mechanism for reduced HDL during calorie restriction may consist of an increased degradation and/or decreased production of HDL particles, as well as calorie restriction, causing a decrease in the production of chylomicron-derived HDL particles [26]. …”
BackgroundPeople may have different responses to the same environmental changes. It has been reported that genome variations may be responsible for these differences. Also, HDL subfractions may be influenced by different genetic variations. The aim of the present study was to determine gene-diet interactions and to evaluate the influence of weight loss on HDL subfractions between two genotypes of -265 T>C APOA-II polymorphism.MethodsIn the present study, 56 overweight and obese patients with type 2 diabetes mellitus were selected from 697 genotype-specified subjects. After matching for gender, age and BMI at the beginning of the study, an equal number of patients remained on each genotype of APOA-II (TT/TC and CC group). After a 6-week calorie restriction program, 44 patients completed the study. Serum HDL subfractions, including HDL2 and HDL3 and LCAT activity, were compared between the two genotypes and, before and after the intervention, were separated in each genotype.ResultsSerum concentration of HDL and its subfractions decreased significantly due to the weight loss. A comparison of the mean changes between the genotypes showed that HDL3 significantly decreased in the CC genotype while, in the TT/TC group, the serum concentration of HDL2 was significantly reduced. However, the increase of LCAT activity was not significant among the two genotypes.ConclusionA comparison of mean changes of variables within two genotype groups showed that C homozygote carriers lead to a general shift toward larger size HDL subfractions and T allele carriers shift toward smaller size HDL subfractions after weight loss.
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