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At least 199 records · Page 11Linked to original sources
PubMed2005

Obesity enhances the induction of plasminogen activator inhibitor-1 by restraint stress: a possible mechanism of stress-induced renal fibrin deposition in obese mice.

BACKGROUND AND OBJECTIVES: Cardiovascular/thrombotic diseases are frequently induced by a variety of stressors. Obese patients are susceptible to thrombotic diseases associated with stress, but the underlying mechanism is still unknown. We have begun to investigate the expression of a primary inhibitor of fibrinolysis, plasminogen activator inhibitor-1 (PAI-1), in association with tissue thrombosis, using restraint-stressed obese mice. METHODS AND RESULTS: We analyzed the expression of PAI-1 after restraint (immobilization) stress in genetically obese mice in comparison with their lean counterparts. Dramatic increases in PAI-1 antigen in plasma and in tissue extracts were observed in the obese mice exposed to restraint stress. The induction of PAI-1 mRNA by stress in the tissues was also pronounced in the stressed obese mice as compared with the lean mice, especially in the hearts and adipose tissues. In situ hybridization analysis revealed that strong signals for PAI-1 mRNA were localized in the adipocytes, cardiovascular endothelial cells, and renal glomerular cells of the stressed obese mice. Histological examination revealed that renal glomerular fibrin deposition was detected only in the obese mice after 2 h of restraint stress. CONCLUSIONS: Obesity enhances the stress-mediated PAI-1 induction in the blood and tissues. This phenomenon may be associated with the increased risk of stress-induced renal fibrin deposition in obese subjects.

Adipocytes↗
PubMed1996

Human obese gene: molecular screening in Japanese and Asian Indian NIDDM patients associated with obesity.

The mouse obese (ob) gene has recently been isolated through the positional cloning technique and has been proved to result in the obese and NIDDM phenotype in mice when mutated (Nature 372:425-432, 1994). More recently, it has been demonstrated, by experiments with recombinant ob protein, that ob gene product can cause mice, including ob/ob mice, diet-induced obesity mice, and normal mice, to lower their food intake and body weight (Science 269:540-549, 1995). To investigate the genetic and/or environmental influences underlying the development of NIDDM associated with obesity, we isolated and partially sequenced the human obese (OB) gene. The human OB gene isolated in this study encoded 167 amino acids and its open reading frame was revealed to be divided into two parts with an intermediate intron of approximately 2.4 kb. Using the single-strand conformation polymorphism (SSCP) technique, we screened Japanese and Asian Indian subjects for mutations in the protein coding regions of the OB gene. A total of 75 NIDDM patients with obesity (54 Japanese and 21 Asian Indians), 40 NIDDM patients without obesity (34 Japanese and 6 Asian Indians), and 34 Japanese patients with simple obesity showed no abnormal SSCP patterns in either component of the coding sequences. These results suggested that mutations in the coding regions of the OB gene are not likely to be commonly identifiable and that there would likely be a kind of obesity-associated NIDDM not caused by mutations of the OB gene.

Adult↗
PubMedDate not supplied

Intragastric balloon: another option for treatment of obesity and morbid obesity.

BACKGROUND/AIMS: The BioEnterics Intragrastric Balloon (BIB, BioEnterics, Santa Barbara, CA) in association with restricted diet has been used for the treatment of obesity and morbid obesity. METHODOLOGY: Since March 1998, 349 BIB were placed in 303 obese and morbidly obese patients; 95 patients were male and 208 female; mean age was 41.5 years (19-70); mean weight was 118.8 Kg (67-229); mean BMI was 42 Kg/m2, % excess weight was 62.3% (4.6-216.3). The balloon was inserted and removed endoscopically under general anesthesia. Patients were given a balanced diet of 1000 Kcal/day. RESULTS: After 4 months of balloon treatment, the mean weight loss was 13.9 Kg and the mean reduction in BMI was 4.8 Kg/m2. Weight loss was greater in male patients. Weight loss was accompanied by an improvement of the diseases associated with obesity, in particular diabetes. CONCLUSIONS: The best indications for BIB were: morbidly obese (BMI >40) and super-obese patients (BMI >50) in preparation for bariatric operations; obese patients with BMI 35-40 with co-morbidity in preparation for bariatric surgery; obese patients with BMI 30-35 with a chronic disease otherwise unresolved; patients with BMI <30 only in a multidisciplinary approach.

Adult↗
PubMed1991

Body weight and longevity in genetically obese and non-obese mice fed fat-modified diets.

Polygenically obese and genetically related non-obese male mice were fed ad libitum purified diets differing in quantity or type of fat from weaning onward to determine effects upon weight gain and life span. Non-obese mice lived 71% longer than mice in the obese line (mean = 753 d versus 441 d). Obese mice fed a low-fat diet containing 1% corn oil by weight lived 26% longer than their obese counterparts fed high fat diets containing 20% additional fat as either corn oil or beef tallow. The low fat diet had more of a normalizing effect upon longevity than upon body weight in polygenically obese mice. Conversely, dietary fat concentration had little effect upon longevity in non-obese mice and more effect upon body weight than in genetically obese mice. Type of dietary fat had little effect upon body weight and no effect upon longevity. The results of this study suggest that life span was only partially explained by body weight, and furthermore, that genetics play a greater role than body weight or dietary fat concentration in determining life span.

Animals↗
PubMed1994

Effects of obesity on bile formation and biliary lipid secretion in the genetically obese JCR:LA-corpulent rat.

Obesity, a known risk factor in cholesterol gallstone disease, is a favorable factor in the formation of bile supersaturated with cholesterol. Previous studies have been indirect and limited to human beings. To better define the hepatic secretory defect, we directly measured bile secretion and bile salt kinetics in a genetically obese rat. Common bile duct cannulations and 24-hr bile collections were performed on 11 obese (homozygous for the cp gene) and 11 lean (heterozygous cp) female rats of the JCR:LA-cp strain. In absolute terms, obese rats had normal bile salt secretion rates, 28% larger bile salt pools and 45% greater bile salt synthesis than lean controls. Obese rats had twice the total liver DNA content of lean controls, indicating twice the liver cell number. In terms relative to liver cell number, bile salt synthesis per milligram DNA was no different in the obese rats and controls. Biliary secretion under basal conditions, when expressed per total DNA content, was significantly decreased in the obese rats. Bile salt and phospholipid secretion per milligram DNA were decreased 54% and 49%, respectively, whereas a lesser 31% reduction in cholesterol secretion resulted in an increased cholesterol saturation index. The bile salt secretion rate and bile flow per milligram DNA were both decreased by half in obese rats, a cholestatic state likely reflecting the accumulation of intracellular microvesicular fat and mitochondrial damage. The secretory defect in this model of obesity is therefore less bile salt and phospholipid in relation to the cholesterol secreted per liver cell.

Animals↗
PubMed1993

Meal-induced thermogenesis in obese children with or without familial history of obesity.

Resting metabolic rate (RMR) and the thermic effect of a meal (TEM) were measured in a group of 26 prepubertal children divided into three groups: (1) children with both parents obese (n = 8, group OB2); (2) children with no obese parents and without familial history of obesity (n = 8, OB0); and (3) normal body weight children (n = 10, C). Average RMR was similar in OB2 and OB0 children (4785 +/- 274 kJ/day vs 5091 +/- 543 kJ/day), but higher (P < 0.05) than in controls (4519 +/- 322 kJ/day). Adjusted for fat-free mass (FFM) mean RMRs were comparable in the three groups of children (4891 +/- 451 kJ/day vs 5031 +/- 451 kJ/day vs 4686 +/- 451 kJ/day in OB2, OB0, and C, respectively). The thermic response to the mixed meal was similar in OB2, OB0 and C groups. The TEM calculated as the percentage of RMR was lower (P < 0.05) in obese than in control children: 10.2% +/- 3.1% vs 10.9% +/- 4.3% vs 14.0% +/- 4.3% in OB2, OB0, and C, respectively. The similar RMR as absolute value as well as adjusted for FFM, and the comparable thermic effect of food in the obese children with or without familial history of obesity, failed to support the view that family history of obesity can greatly influence the RMR and the TEM of the obese child with obese parents.

Basal Metabolism↗
PubMedDate not supplied

Overall obesity and abdominal obesity and the risk of metabolic abnormalities.

BACKGROUND: Obesity is a risk factor for multiple chronic diseases. AIM: To determine the relationship between overall or abdominal obesity and various metabolic abnormalities. METHODS: The medical records of participants undergoing examination from January 2000 to December 2002 were analysed. Body mass index (BMI; kg/m2) for overall obesity and waist circumference (WC; cm) indicating abdominal obesity were measured. Four groups were studied: (1) BMI < 27kg/m2, WC: female < 80cm or male < 90cm; (2) BMI > or = 27kg/m2, WC: female < 80cm or male < 90cm; (3) BMI < 27kg/m2, WC: female > or = 80cm or male > or = 90cm; (4) BMI > or = 27kg/m2, WC: female > or = 80cm or male > or = 90cm. RESULTS: There were 1,342 (44%) females and 1,711 males aged 20-87 years. The prevalence of overall obesity was 20.4% and abdominal obesity was 48%. Obese subjects had more metabolic abnormalities than non-obese in terms of risk of hypertension, hyperglycaemia, hypercholesterolaemia, hypertriglyceridaemia, high level of LDL, low level of HDL, high ratio of TC/HDL, hyperuricaemia and fatty liver. CONCLUSIONS: As overall and abdominal obesity may predict clustering of metabolic abnormalities we suggest that BMI and WC are convenient methods for assessing metabolic abnormalities in primary healthcare settings.

Abdominal Fat↗
PubMed2003

Kinetics of catecholamines and potassium, and heart rate during exercise testing in obese subjects. Heart rate regulation in obesity during exercise.

BACKGROUND: Obesity is characterised by a marked insulin resistance which involves an abnormal regulation of K(+) uptake and metabolism. Less is known about the effect of physical exercise on K(+) kinetics. AIM OF THE STUDY: To assess plasma catecholamines and potassium levels and their relationship with cardiac activity during a physical effort up to exhaustion in young obese subjects. METHODS: Blood samples for epinephrine (E), norepinephrine (NE), potassium (K+) and heart rate (HR) were collected at the end of every step during a progressive cycloergometric test up to exhaustion in twelve obese subjects (6 males, aged 26+/-2, BMI 39.9+/-1) and twelve normal subjects (6 males, aged 28.2+/-2, BMI 22+/-1). In every subject anaerobic threshold (AT) was detected. RESULTS: In obese subjects plasma catecholamines rose faster but had a lower peak in correspondence of maximal work-loads, with respect to controls. Catecholamines had a linear correlation in the obese group and a quadratic one in the control group when plotted vs O(2) consumption. The increase of plasma potassium was less in obesity than in control. CONCLUSIONS: During physical exercise K(+) and catecholamines kinetics differ significantly in obese subjects vs normals and they may justify a less prompt cardiac response at the higher work-loads and a lower work capacity. The present data can be interpreted in the light of the insulin resistance syndrome of obesity, which causes an abnormal regulation of the Na-KATPase and of K(+) channels during physical exercise. The results of the present study may be relevant to nutritionists when suggesting physical exercise to obese subjects.

Adult↗
PubMed1983

Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes.

Male, 5 months old, massively obese, spontaneously hypertensive rats (Obese/SHR) were given 10 mg alloxan/100 g b.w., s.c., to induce diabetes. Control Obese and non-obese/SHR were given saline. Insulin therapy was withheld. All of the animals were killed at 6 months of age. Alloxan caused a slight but statistically significant increase in blood pressure, pituitary and adrenal glandular hyperplasia, hyperlipidemia, hyperglycemia, and increased BUN levels. The giant sized islets of Langerhans in Obese/SHR showed only partial degranulation of the insulin-producing beta cells concomitant with residual but apparently adequate blood insulin levels, whereas the islets of non-obese/SHR exhibited virtually total beta cell degranulation and only trace amounts of blood insulin. The alloxanized, non-obese rats were severely emaciated; the alloxanized Obese/SHR maintained their obesity. Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process. The genetically-programmed pathogenesis of diabetes, obesity, hypertension, and Cushingoid pathophysiology of Obese/SHR may be due to hyperadrenocorticism.

Adrenal Cortex↗
PubMed1995

Beta-adrenergic stimulation and abdominal subcutaneous fat blood flow in lean, obese, and reduced-obese subjects.

The present study was designed to investigate whether the beta-adrenergically mediated blood flow response of abdominal subcutaneous adipose tissue (per unit adipose tissue weight) was altered in obesity and to study the effect of weight reduction on this response. Body composition (underwater weighing) and fat blood flow were determined in a group of lean (n = 9; % body fat, 11.6 +/- 3.9) and obese (n = 9; % body fat, 28.3 +/- 1.8) subjects. In seven obese subjects, measurements were also performed after a 4-week period of weight reduction induced by a very-low calorie diet (% body fat after diet 23.4 +/- 3.3). After an overnight fast, abdominal subcutaneous fat blood flow was determined by the 133xenon washout technique during a 30-minute period of supine rest and during 30-minute periods of infusion of the beta-agonist isoprenaline (ISO) with and without simultaneous infusion of the beta 1-blocker atenolol (AT). Basal abdominal fat blood flow was significantly higher in lean as compared with obese subjects, whereas weight reduction significantly increased basal fat blood flow (obese v reduced-obese, P < .05). There was a significant increase in abdominal fat blood flow as a result of ISO infusion in lean and obese subjects before and after weight reduction. During ISO+AT infusion, abdominal fat blood flow was still significantly increased as compared with control values in lean and obese subjects. The increase in blood flow during ISO was significantly higher in lean subjects than in obese subjects, whereas the ISO+AT-induced blood flow response was comparable.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Muscles↗
PubMed2004

Laparoscopic Roux-en-Y gastric bypass in morbidly obese and super morbidly obese patients.

BACKGROUND: Our objective was to compare the outcomes after laparoscopic Roux-en-Y gastric bypass (RYGB) in morbidly obese (body mass index [BMI] <50) patients with super morbidly obese (BMI >50) patients. METHODS: A prospective analysis of 120 patients who underwent laparoscopic RYGB at a community based teaching hospital between January 2002 and August 2002 was performed. Sixty patients with BMI <50 were compared with 60 patients with BMI >50. Study endpoints included: operative time, length of stay, and overall complication rates including early (<7 days) and late (>7 days) complications. RESULTS: Mean BMI in the obese group was 44.6 (range 39 to 49) versus 58.6 (range 50 to 100) in the superobese group. Medical comorbidities, age, and sex distribution were similar in both groups. Mean operative time in the obese group was 128 minutes (range 75 to 225) versus 144 minutes (range 75 to 240) in the superobese group. The overall complication rate was 10% in the obese group versus 20% in the superobese group. (P = 0.2) With regard to the obese group, the early complication rate was 5% (n = 3). These included 2 upper gastrointestinal bleeds and 1 respiratory failure. The late complication rate in this group was also 5% (n = 3). These were all anastomotic strictures requiring endoscopic dilation. In comparison, in the superobese group, the early complication rate was 8% (n = 5). These included 2 upper gastrointestinal bleeds, 1 pneumonia, 1 superficial wound infection, and 1 small bowel obstruction. The late complication rate in this group was 12% (n = 7). These included 4 anastomotic strictures, 1 incisional hernia, 1 pulmonary embolism, and 1 anastomotic leak. There were no conversions to open gastric bypass or deaths in either group. Median length of stay in both groups was 2 days. CONCLUSIONS: Our data demonstrate no significant difference in operative times, complication rates or length of stay between morbidly obese and super morbidly obese patients undergoing laparoscopic RYGB. Laparoscopic RYGB is safe and technically feasible in the super morbidly obese patient population.

Adult↗
PubMed2006

Colorectal cancer screening among obese versus non-obese patients in primary care practices.

BACKGROUND: Obesity is associated with increased colorectal cancer incidence and mortality. Previous studies using telephone survey data showed that obese women were less likely to receive colorectal cancer screening. It is unknown if this is true among patients in primary care practices. METHODS: Retrospective chart reviews were conducted in 2003-2004 of men and women in 22 suburban New Jersey and Pennsylvania primary care practices. Data from patients age 50 years and over (n=1297) were analyzed using hierarchical logistic regression. The outcome measure was receipt of colorectal cancer screening (fecal occult blood test within 1 year, sigmoidoscopy within 5 years, colonoscopy within 10 years, or barium enema within 5 years) among obese and non-obese patients. RESULTS: Overall, 39% of patients were obese and 29% received colorectal cancer screening. After controlling for age, gender, total number of co-morbidities, number of visits in the past 2 years, and number of years in the practice, obese patients had 25% decreased odds of being screened for colorectal cancer compared to non-obese patients (OR 0.75, 95% CI, 0.62-0.91). The relationship of obesity and colorectal cancer screening did not differ according to gender. Number of visits (OR 1.04, 95% CI, 1.01-1.06) and male gender (OR 1.53, 95% CI, 1.19-1.97) was associated with increased odds of receiving colorectal cancer screening. CONCLUSION: Identification of physician and patient barriers to colorectal cancer screening is needed, particularly in obese patients, so that effective interventions may be developed to increase screening in this high-risk group.

Aged↗
PubMed2004

The evaluation of plantar pressure distribution in obese and non-obese adults.

BACKGROUND: Although previous studies have generally reported increased plantar pressure values with obesity, none of these studies has classified the obesity. Our aim in this study was to compare the plantar pressure distribution in obese and control adults during standing and walking. METHODS: This study was performed on 100 feet of 50 study participants. The subjects gathered in two groups, each containing 25 study participants, as non-obese and class 1 obese according to their body mass index values. Static and dynamic pedobarographic evaluations were performed during standing and walking. The findings were compared between the groups and also the correlation of body mass index with the pedobarographic parameters was assessed. FINDINGS: The static pedobarographic evaluation revealed significantly higher values in terms of forefoot peak pressure, total plantar force and total contact area in the feet of class 1 obese subjects when only middle foot peak pressure was found to be higher in class 1 obese subjects than controls as a dynamic pedobarographic parameter. Among the static parameters body mass index was found to have positive correlation with total plantar force (r=0.50, P=0.000) and total contact area (r=0.33, P=0.019). Only middle foot peak pressure (r=0.32, P=0.025) among the dynamic pedobarographic parameters had positive correlation with body mass index. INTERPRETATION: This study may be a first step to evaluate the effect of different obesity categories on the plantar pressure values. Further studies are needed to investigate the effect of different obesity grades.

Female↗
PubMed2005

Obesity and extreme obesity, manifest by ages 20-24 years, continuing through 32-41 years in women, should alert physicians to the diagnostic likelihood of polycystic ovary syndrome as a reversible underlying endocrinopathy.

OBJECTIVES: Document obesity-extreme obesity in most 20-24, 25-29, and 32-41 years old women with PCOS as a stimulus for physicians to consider the diagnosis of PCOS, an underlying reversible endocrinopathy. STUDY DESIGN: In matched age groups 20-24, 25-29, and 32-41 years, we compared BMI in 84, 129, and 188 Caucasian women with PCOS versus 956, 815, and 815 women in NHANES I (general population), and 25, 36, and 45 non-pregnant women (community obstetrics practice). RESULTS: At ages 20-24, 25-29, and 32-41 years, mean+/-S.D. BMIs in women with PCOS (35.3+/-7.7, 36.0+/-9.4, 36.7+/-8.2) were much greater than NHANES I (22.8+/-4.6, 23.3+/-5.0, 24.5+/-5.6; p < .0001), and community (26.1+/-6.8, 26.9+/-6.6, 25.2+/-5.2; p < .0001). Classifying BMI <25 (normal), > or =25-30 (overweight), > or =30-40 (obese), > or =40 (extremely obese), at ages 20-24, 25-29, and 32-41 years: 76, 73, and 78% of PCOS women were obese-extremely obese, versus 7, 11, and 14% of NHANES I, and 20, 28, and 15% of community women. At ages 20-24, 25-29, and 32-41 years, only 10, 12, and 7% PCOS women had BMIs <25, versus 78, 74, and 66% NHANES I, and 48, 47, and 58% of community women. CONCLUSIONS: Obesity-extreme obesity in women, manifest by ages 20-24 years, continuing through 32-41 years, should alert physicians to the likelihood of PCOS, an underlying, heritable, potentially reversible, insulin resistant endocrinopathy that promotes obesity.

Adult↗
PubMed2005

The link between obesity and the built environment. Evidence from an ecological analysis of obesity and vehicle miles of travel in California.

AIMS: Obesity and physical inactivity are known to be risk factors for many chronic diseases including hypertension, coronary artery disease, diabetes, and cancer. We sought to explore the association between an indicator of transportation data (Vehicle Miles of Travel, VMT) at the county level as it relates to obesity and physical inactivity in California. METHODS: Data from the California Health Interview Survey 2001 (CHIS 2001), the US 2000 Census, and the California Department of Transportation were merged to examine ecological correlations between vehicle miles of travel, population density, commute time, and county indicators of obesity and physical inactivity. Obesity was measured by body mass index (BMI). Physical inactivity was based on self-reported behaviors including walking, bicycling, and moderate to vigorous activity. The unit of analysis was the county. Thirty-three counties in California with population size greater than 100,000 persons per county were retained in the analyses. RESULTS: CHIS 2001 statewide obesity prevalence ranged from 11.2% to 28.5% by county. Physical inactivity ranged from 13.4% to 35.7%. Daily vehicle miles of travel ranged from 3.3 million to 183.8 million per county. By rank bivariate correlation, obesity and physical inactivity were significantly associated (p<0.01). Furthermore, by rank analysis of variance, the highest mean rank obesity was associated with the highest rank of VMT (p<0.01). Similar rank patterns were observed between obesity and physical inactivity and commute time. Associations between VMT and physical inactivity were examined but failed to reach statistical significance. CONCLUSION: This analysis adds to the growing evidence supporting the association between VMT (a measure of automobile transportation) and obesity. An urban design characterized by over dependence on motorized transportation may be related to adverse health effects.

Adolescent↗
PubMed2006

Angiotensinogen gene polymorphism (Met235Thr) influences visceral obesity and insulin resistance in obese Japanese women.

To investigate the relationship between angiotensinogen (AGT) Met235Thr polymorphism (M235T) and human obesity, because AGT is regarded as one of the cytokines produced from adipocytes and serum AGT concentrations are reported to be positively correlated with body mass index. One hundred and twenty obese Japanese women (age, 58.8+/-9.4 years; body mass index, 32.2+/-4.9 kg/m(2)) were enrolled. Angiotensinogen genotypes were determined with a fluorescent allele-specific DNA primer assay system. Subjects were divided into M/M, M/T, and T/T groups. Control subjects comprised 146 healthy age-matched women. Clinical characteristics and the effects of diet and exercise therapy for 6 months were compared among the 3 genotypes. The genotype frequencies of AGT M235T polymorphism were in accordance with the Hardy-Weinberg equation (obese: M/M, 6.7%; M/T, 27.5%; T/T, 65.8%; control: M/M, 6.8%; M/T, 21.2%; T/T, 71.9%). The frequency of the T allele did not differ between obese and control subjects (0.80 vs 0.83). As the number of obese women with M/M genotype was only 8, comparisons of the characteristics and outcomes of weight reduction therapy were performed only between subjects with M/T genotype and T/T genotype. In the T/T group, % body fat and waist circumference at baseline were significantly greater than in the M/T group (36.3%+/-4.8% vs 33.8%+/-4.7%, P=.0105; 107.9+/-10.9 vs 102.6+/-7.9 cm, P=.0428, respectively). Before the weight reduction therapy, significantly higher insulin and higher homeostasis model assessment (HOMA-R) were demonstrated in the T/T group than in the M/T group (9.1+/-5.5 microU/mL vs 5.9+/-4.4 microU/mL, P=.0056; 2.3+/-1.4 vs 1.6+/-1.3, P=.0252, respectively). Both systolic and diastolic blood pressure at baseline in the T/T group tended to be higher than those in the M/T group, but the differences were not significant. No genotype-dependent difference in energy expenditure or outcome of weight reduction therapy was observed with respect to AGT M235T polymorphism. After the diet and exercise therapy, the blood pressure in the T/T group tended to be higher than that in the M/T group, but the difference was not significant. We demonstrated that the T/T genotype of the AGT M235T gene polymorphism was positively related to visceral obesity and hyperinsulinemia in obese Japanese women. Blood pressure did not show genotype-specific differences before or after the treatment. Further studies of the association between obesity and this gene polymorphism should contribute to understanding and treating obesity-related diseases.

Aged↗
PubMed1998

The in vitro oxidizability of lipoprotein particles in obese and non-obese subjects.

There exists much evidence suggesting a major role for the oxidized low density lipoprotein (LDL) and VLDL particles in the pathogenesis of atherosclerosis. Although obesity is characterized by dyslipidemia, less is known about the oxidation capacity of lipoproteins in obese subjects. We measured the oxidizability in vitro in 21 premenopausal women with a BMI of 36.7+/-5.4 and compared them to 18 age-matched controls (BMI 21.9+/-1.8). The oxidizability of the non-HDL fraction is evaluated by measuring the fluorescence and thiobarbituric acid reactive substances (TBARS; MDA nM/mg non-HDL) at different time intervals of incubation. TBARS formation increased linearly with the increase of lipids both in non-obese and obese subjects. TBARS, measured every 30 min, increased in non-obese controls up to a maximum of 59.6 at 180' in contrast to a maximum of 77.1 at 180' (P < 0.001) in obese, but healthy, normocholesterolemic subjects. At each measurement the TBARS were significantly higher (P < 0.01-0.001) in obese subjects. Also the lag-time (period from zero to the start of the particle oxidation process) was significantly lower (92.5 vs. 123.4; P < 0.001) in obese subjects, when compared to lean controls. BMI correlates significantly with TBARS formation and its log transformed values (maximum P < 0.001). The lag-time was negatively related (n=39 total group, r=- 0.57, P < 0.001) to body weight and BMI. A significant relationship exists between TBARS formation (up to r=0.59) and triglyceride levels and a negative relationship exists with HDL-cholesterol levels. In vitro oxidizability of non-HDL lipoproteins is significantly increased in obese, non-diabetic subjects and related to increased body weight and triglyceride levels. Further studies are necessary to explore the underlying mechanisms for this phenomenon.

Adult↗
PubMed2003

Mutations in the adiponectin gene in lean and obese subjects from the Swedish obese subjects cohort.

Adiponectin (also called AdipoQ, gelatin-binding protein 28, Acrp30) DNA sequence variants were determined in 96 unrelated female subjects with severe obesity (mean body mass index [BMI], 42.3 kg/m2) and in 96 non-obese female controls (mean BMI, 23.0 kg/m2) from the Swedish Obese Subjects (SOS) cohort. A single base substitution (T45G) at codon 15 of exon 2 resulting in no change in amino acid (Gly15Gly) was found in equal frequencies among obese and control subjects. However, this polymorphism was associated with serum cholesterol and waist circumference (P=.023 and.043, respectively) in the obese group. A IVS2 + G62T sequence variation was also identified, but had similar prevalence rates in obese and control subjects. Blood glucose was highest in the obese female subjects who were homozygotes for the G allele (GG) of the IVS2 + G62T polymorphism (N=56; P=.033) and all the diabetics (n=6) in this sample were in this group. IVS2 + G62T polymorphism was also associated with BMI (P=.014), diastolic blood pressure (P=.009), and sagittal diameter (P=.032). A missense point mutation at codon 111 (Tyr111His) was not associated with any obesity-related phenotypes. In conclusion, adiponectin DNA sequence variations might play a role in the complications of morbid obesity and should be further investigated.

Adiponectin↗