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PubMed1990

Patterns of food use and nutrient intake of obese and non-obese Hualapai Indian women of Arizona.

To document patterns of food use and nutrient intake associated with obesity in Native American women, a sample of 14 obese and 14 non-obese free-living Hualapai Indian women living in northwest Arizona was studied. Patterns of food use were determined through long-term observation, dietary histories, and 24-hour dietary recalls. Dietary intake was determined through 24-hour dietary recalls over 7 consecutive days. Patterns of food acquisition, selection, and preparation were similar for obese and non-obese Hualapai women. The diets of both groups were dominated by nonalcoholic beverages, potatoes, beans, white wheat flour, and canned goods. Wild and locally cultivated foods were not eaten on a regular basis. The diets of both the obese and non-obese women were high in energy (pooled mean +/- standard deviation [SD] = 2,602 +/- 766 kcal/day) and carbohydrates (pooled mean +/- SD = 333.4 +/- 95.6 gm/day), moderate in protein (pooled mean +/- SD = 77.8 +/- 20.9 gm/day) and fat (pooled mean +/- SD = 101.1 +/- 25.4 gm/day), and low in crude fiber (pooled mean +/- SD = 4.7 +/- 2.0 gm/day). The study indicates that significantly (p less than .001) higher energy intakes of the obese women can be attributed to their greater consumption of nonalcoholic and alcoholic beverages.

Adult↗
PubMed1989

TSH, thyroid hormones and nuclear-binding of T3 in mononuclear blood cells from obese and non-obese women.

The specific nuclear-binding of T3 (NBT3) in mononuclear blood cells, and the concentrations of TSH, thyroid hormones, and binding proteins were measured after overnight fasting in 12 obese and in 14 non-obese women, none of the subjects were taking any medicine. The concentrations of TSH and free plus bound-T3 (TT3) were significantly higher in the obese (p less than 0.05), concentrations of T4 and binding proteins did not differ. The NBT3 was significantly lower in the obese women; the maximal binding capacity (MBC) was 34.5 +/- 11.6 fmol/mg DNA in the obese subjects and 50.0 +/- 11.6 fmol/mg DNA in the non-obese subjects (p less than 0.02). The binding affinities did not differ. We have previously shown that increasing T3 concentrations within the physiological range down-regulates NBT3. Therefore, the reduced NBT3 in the obese women was probably secondary to the increased TT3 concentration and was not caused by a primary tissue resistance. The higher TSH and TT3 in the obese women could be caused by a greater caloric intake.

Adult↗
PubMed1986

Liver function in moderate obesity--study in 534 moderately obese subjects among 4613 male company employees.

The influence of moderate obesity on the liver was assessed in 4613 male company employees including 534 moderately obese subjects (30-50 percent overweight). Serum levels of transaminases and gammaglutamyl transferase activities were significantly higher in moderately obese male non-drinkers than in non-obese non-drinkers. Twenty-four percent of male non-drinkers with moderate obesity had abnormal levels of sGPT and 47 percent of moderately obese male non-drinkers had significant hepatic steatosis as assessed by computed tomography. Although most previous studies on this subject were concerned with morbid obesity accompanying only those of more than 50 percent overweight or those who required surgery, the results of this study clearly indicate that moderately obese subjects also have frequent liver dysfunction.

Alanine Transaminase↗
PubMed1987

Obesity as a risk factor in drug-induced organ injury: increased liver and kidney damage by acetaminophen in the obese overfed rat.

The overfed rat served as the animal model for examining the influence of obesity on the hepatotoxic and nephrotoxic potential of metabolically activated drugs, and acetaminophen served as the prototype drug. Weanling Sprague-Dawley rats were given a standard pellet diet or semisynthetic, energy-dense diet designed to produce obesity. After 24 weeks, when overfed rats outweighed controls by more than 50%, animals received 710 mg/kg of acetaminophen i.p., based on total body weight. Toxicity evaluation included biochemical signs of organ injury over the first 24 hr and histopathologic changes in tissue morphology at 48 hr. Both enzyme release (alanine aminotransferase into plasma, alkaline phosphatase into urine) and frank cellular necrosis in liver and kidney of obese rats greatly exceeded that in pellet-fed controls. Contributing to the potentiation of injury were higher peak plasma concentrations of acetaminophen in obese animals resulting from total body weight dosing. However, liver and kidney injury and mortality remained elevated when peak plasma concentrations were matched by fat-free mass dosing, indicating that increased toxicity also was related to obesity. Incomplete recovery of acetaminophen and metabolites from obese animals (45 vs. 71% in control rats) caused by a functional renal impairment made it impossible to determine the metabolic fate of acetaminophen in overfed animals from the analysis of urine collections. Drug products measured in urine were summed with amounts remaining in carcass at sacrifice, computed as terminal plasma concentrations times respective distribution volumes. These results showed obese rats to form more glucuronide and less sulfate conjugate than did pellet-fed controls, coinciding with clinical evidence for enhanced glucuronidation in obese humans.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1994

The natural history of obesity in an obese population and associations with metabolic aberrations.

The natural history of obesity was examined in a nation-wide sample of 1,084 obese men and 1,367 obese women aged 37-59 years who were recruited into a registry of potential subjects for an intervention trial. The registry and intervention studies are jointly referred to as SOS ('Swedish Obese Subjects'). In the registry, the mean body mass index was 37.7 kg/m2 in men and 40.9 kg/m2 in women. Descriptive information on subjects' weight histories and the relative weights of their biological parents was collected by means of a self-administered questionnaire. At a physical examination shortly thereafter, weights, heights and selected cardiovascular risk factors were measured in the fasting state. Virtually all subjects reported weight loss attempts in the past, men and women reported having gained weight during adulthood at a considerably higher rate than that observed in population-based samples. Significant correlations were observed between relative weights of obese males and both of their biological parents, but not between obese women and either of their parents. Indices of medical risk were then examined in relation to individual weight histories. Familial predisposition did not relate to most aspects of current medical risk. However, later-onset obesity tended to be associated with greater cardiovascular risk, while prior weight loss was predictive of an improved risk factor profile. These latter associations were not dependent on a subject's current degree of obesity and were particularly consistent with respect to fasting insulin level.

Adult↗
PubMed1993

Swedish obese subjects (SOS)--an intervention study of obesity. Baseline evaluation of health and psychosocial functioning in the first 1743 subjects examined.

This part of an on-going intervention trial analyses impacts of obesity on psychosocial factors and health. The study sample comprised 800 obese men (BMI > or = 34 kg/m2) and 943 women (BMI > or = 38 kg/m2) ranging in age from 37 to 57 years. All participants completed standardized health-related quality of life measures, a validated obesity-specific eating inventory and study-specific questionnaires on current and past health status, use of medical care and medications, socioeconomic status, dietary habits, physical activity habits, weight history and familial history of obesity. Chronic patients and population samples were used as reference. The obese reported distinctly poorer current health and less positive mood states than the reference subjects, women being worse than men. Anxiety and/or depression on a level indicating psychiatric morbidity were more often seen in the obese and again women reported more affliction than men. Furthermore, the average poor mental well-being was worst than in chronically ill or injured patients, such as rheumatoid, cancer survivors and spinal cord injured persons. Predictors of perceived health and psychosocial functioning could be discerned using a comprehensive system of statistical analyses (16-28% explained variance). A background of both somatic and psychiatric morbidity was decisive for the health and psychosocial functioning in the obese; joint symptoms and angina pectoris dominated among somatic variables. Physical inactivity was the most prominent of traditional risk factors. The number of dieting attempts and body image were important weight correlates. Our results provide further evidence to the effect that severe obesity is a crippling condition.

Adult↗
PubMed1997

Variation in adrenergic regulation of lipolysis between omental and subcutaneous adipocytes from obese and non-obese men.

Regional variations in adipocyte lipolysis between subcutaneous and visceral fat may be important for obesity complications. In the present study, we compared adrenergic regulation of lipolysis in omental and subcutaneous adipocytes from obese (n = 15) and non-obese (n = 14) male subjects. Waist-to-hip ratio, blood pressure, plasma insulin, and plasma triglycerides were increased in obesity. No regional differences in adrenoceptor lipolytic function were observed in non-obese subjects with the exception of a slight increase in noradrenaline sensitivity in omental adipocytes (P < 0.05), because of increased beta(1)-adrenoceptor sensitivity (P < 0.05). In the obese subjects, the rate of noradrenaline-induced glycerol release was 2-fold higher (P < 0.005) and the noradrenaline sensitivity was 3-fold higher (P < 0.05) in omental versus subcutaneous adipocytes. These findings were mainly due to a 50-fold increase in omental beta(3)-adrenoceptor sensitivity (P < 0.002) and to a smaller 6-fold increase in omental beta(1)-adrenoceptor sensitivity (P < 0.02), accompanied by increased beta(3)- as well as beta(1)-adrenoceptor lipolytic rates at approximately 50% receptor subtype occupancy by the agonist (P < 0.05). In conclusion, minor regional differences in adipocyte lipolytic response to catecholamines are present in non-obese males. In contrast, catecholamine-induced lipolysis is markedly increased in omental as compared to subcutaneous adipocytes in obese males, mainly due to an increase in beta(3)-adrenoceptor function of visceral fat cells, in combination with a smaller increase in beta(1)-adrenoceptor function.

Adipocytes↗
PubMed2024

Dissecting the anti-obesity components of ginseng: How ginseng polysaccharides and ginsenosides target gut microbiota to suppress high-fat diet-induced obesity.

INTRODUCTION: Ginseng demonstrates therapeutic potential in treating obesity, with both experimental and clinical studies suggesting its anti-obesity effects are mediated by gut microbiota. Nonetheless, the specific chemical components responsible for this effect remain largely unidentified. OBJECTIVES: This study aims to investigate the anti-obesity effects and mechanisms of ginseng polysaccharides (GP) and ginsenosides (GS), the primary chemical components of ginseng, with a focus on their impact on gut microbiota. METHODS: The impact of GP and GS on high-fat diet (HFD)-induced obesity was assessed using a mouse model. Molecular mechanisms were explored through a combination of chemical analysis, metagenomics, RT-qPCR, ELISA, and biochemical assays. RESULTS: GP or GS administration effectively prevented adiposity in HFD-fed mice, and both effects were mediated by gut microbiota. Chemical analysis revealed diverse glycosyl groups in GP and GS. Metagenomics data suggested that GP-enriched species, e.g., Bacteroides stercorirosoris and Clostridiales bacterium encoded carbohydrate-active enzymes GH35, GH43 and PL9_1, while GS-enriched Sulfurospirillum halorespirans encoded GH16_5. These enzymes facilitated the utilization of glycosyl groups in GP and GS, selectively stimulating bacterial growth and reshaping the gut microbiota. Furthermore, bacterial species enriched by GP or GS encoded specific functional genes involved in short-chain fatty acid (SCFA) synthesis (K00625 and K00925 for GP; K18118, K00100, and K18122 for GS) and intestinal gluconeogenesis (IGN) (K01678, K00024, and K01596 for GP; K18118 and K00278 for GS). Consequently, the SCFA-GLP-1/PYY signaling and IGN were activated by both GP and GS to ameliorate obesity phenotypes. CONCLUSION: GP and GS, containing diverse glycosyl groups, selectively stimulate specific gut bacteria, triggering mechanisms involved in SCFA-GLP-1/PYY signaling and IGN activation to reduce adiposity in HFD-fed mice. The study enhances understanding of the chemical components crucial for the gut microbiota-mediated anti-obesity effect of ginseng. The mechanistic understanding provides valuable insights for developing ginseng-based drugs or health products to combat obesity.

Gastrointestinal Microbiome↗
PubMed2004

Differences in the pharmacokinetics of peroxisome proliferator-activated receptor agonists in genetically obese Zucker and sprague-dawley rats: implications of decreased glucuronidation in obese Zucker rats.

Genetically obese Zucker rats exhibit symptoms similar to those of obese patients with insulin-resistance or Type II diabetes; therefore, they have been used as a genetic model to study obesity, as well as a pharmacological model for the discovery of new drugs for the treatment of Type II diabetes and hyperlipidemia. In the present study, we compared the pharmacokinetics of two novel peroxisome proliferator-activated receptor (PPAR) agonists, MRL-I [(2R)-7-[3-[2-chloro-4-(4-fluorophenoxy)phenoxy]propoxy]-2-ethyl-3,4-dihydro-2H-benzopyran-2-carboxylic acid] and MRL-II [(2R)-7-[3-[2-chloro-4-(2,2,2-trifluoroethoxy)phenoxy]propoxy]-3,4-dihydro-2-methyl-2H-benzopyran-2-carboxylic acid], in obese Zucker and lean Sprague-Dawley rats following a single intravenous administration. The plasma clearance of both MRL-I and MRL-II was significantly lower in obese Zucker rats (4- and 2-fold, respectively) compared with Sprague-Dawley rats, but without any significant change in the volume of distribution, which resulted in a dramatic increase in the half-life (7- and 3-fold, respectively). The reversible in vitro plasma protein binding of [(14)C]MRL-I and [(14)C]MRL-II was comparable in the two strains, approximately 96% bound. The expression levels of uridine diphosphate-glucuronosyltransferases 1A1, 1A6, 2B1, and CYP2C11 and 3A1 mRNA in liver were lower (30-50%) in Zucker compared with Sprague-Dawley rats, as were the liver glutathione S-transferases (70%), quinone reductase (30%), organic anion-transporting protein 2 (80%), and multidrug resistance-associated protein 2 (Mrp2) (50%) mRNA levels. However, Mrp3 mRNA levels were similar in both strains. Consistent with these observations, the intrinsic clearance (CL(int)), calculated from the V(max)/K(m) of glucuronidation of [(14)C]MRL-I and [(14)C]MRL-II in liver microsomes, was approximately 2-fold lower in obese Zucker rats; the K(m) values were comparable in the two strains for both compounds. In conclusion, differences in the pharmacokinetics of two novel PPAR agonists, both cleared, predominantly, by conjugation, were evident in genetically obese Zucker rats compared with Sprague-Dawley rats. These differences were consistent with changes in the mRNA levels of hepatic drug-metabolizing enzymes and transporters. This information should be considered when comparing pharmacokinetic and efficacious doses in the obese Zucker rats, used as a pharmacological model, with those in Sprague-Dawley rats, which are used widely for drug metabolism and toxicology studies.

Animals↗
PubMed1998

Leptin receptor gene in a large cohort of massively obese subjects: no indication of the fa/fa rat mutation. Detection of an intronic variant with no association with obesity.

The massive obesity caused in rodents by the disruption of the leptin-receptor signal through genetic defects at the level of either leptin (OB) or leptin receptor (OB-R) has raised the question of the relevance of these genes to morbid obesity in humans. In this study, we screened a large population of massively obese subjects for the presence of a leptin receptor mutation homologous to that of fa/fa rats, a single base substitution changing glutamine 269, a highly conserved glutamine found at position 270 in the human sequence. After polymerase chain reaction (PCR) amplification of a DNA region encompassing the end of exon 5, intron 5, and the beginning of exon 6, we performed restriction fragment length polymorphism analysis. Within the limitations of this approach where only mutations introducing restriction sites (5 of 8 possibilities) could be assessed, no evidence of mutation at the codon gln 270 was found in 343 massively obese subjects. However, a new OB-R gene variant in intron 5 was revealed by MaeII digestion of the PCR products. MaeII/hOB-R genotyping revealed no difference in the distribution of the genotypes between obese subjects and a group of 79 unrelated nonobese control subjects. In addition, no significant association between various obesity-related metabolic phenotypes and the presence of MaeII/hOB-R alleles was found. Thus, our results did not support a significant role for the MaeII/hOB-R gene variant in the development of the obese phenotype in the population we studied.

Adult↗
PubMed1999

The yellow mouse obesity syndrome and mechanisms of agouti-induced obesity.

The yellow mouse obesity syndrome is due to dominant mutations at the Agouti locus, which is characterized by obesity, hyperinsulinemia, insulin resistance, hyperglycemia, hyperleptinemia, increased linear growth, and yellow coat color. This syndrome is caused by ectopic expression of Agouti in multiple tissues. Mechanisms of Agouti action in obesity seem to involve, at least in part, competitive melanocortin antagonism. Both central and peripheral effects have been implicated in Agouti-induced obesity. An Agouti-Related Protein (AGRP) has been described recently. It has been shown to be expressed in mice hypothalamus and to act similarly to agouti as a potent antagonist to central melanocortin receptor MC4-R, suggesting that AGRP is an endogenous MC4-R ligand. Mice lacking MC4-R become hyperphagic and develop obesity, implying that agouti may lead to obesity by interfering with MC4-R signaling in the brain and consequently regulating food intake. Furthermore, food intake is inhibited by intracerebroventricular injection of a potent melanocortin agonist and was reversed by administration of an MC4-R antagonist. The direct cellular actions of Agouti include stimulation of fatty acid and triglyceride synthesis via a Ca(2+)-dependent mechanism. Agouti and insulin act in an additive manner to increase lipogenesis. This additive effect of agouti and insulin is demonstrated by the necessity of insulin in eliciting weight gain in transgenic mice expressing agouti specifically in adipose tissue. This suggests that agouti expression in adipose tissue combined with hyperinsulinemia may lead to increased adiposity. The roles of melanocortin receptors or agouti-specific receptor(s) in agouti regulation of adipocyte metabolism and other peripheral effects remain to be determined. In conclusion, both central and peripheral actions of agouti contribute to the yellow mouse obesity syndrome and this action is mediated at least in part by antagonism with melanocortin receptors and/or regulation of intracellular calcium.

Agouti Signaling Protein↗
PubMed2000

Quantitative trait loci for obesity and insulin resistance (Nob1, Nob2) and their interaction with the leptin receptor allele (LeprA720T/T1044I) in New Zealand obese mice.

AIMS/HYPOTHESIS: To locate genes responsible for obesity and insulin resistance, a backcross model of New Zealand obese (NZO) mice with the lean Swiss/Jackson Laboratory (SJL) strain was stablished. RESULTS: In female NZO x F1 backcross mice, two major quantitative trait loci for variables of obesity (body weight, body mass index, total body fat) and insulin resistance (hyperinsulinaemia) were identified on chromosomes 5 (Nob1) and 19 (Nob2) close to the markers D5Mit392 and D19Mit91. The aberrant alleles have presumably contributed by the NZO genome. Whereas Nob1 contributed mainly to higher body weight, Nob2 seemed to mainly aggravate insulin resistance independent of obesity. The leptin receptor variant of NZO (LeprA720T/T1044I) failed to alter any of the variables of obesity. It seemed, however, to enhance the effect of Nob1 on body weight and that of Nob2 on serum insulin concentration. When expressed in COS-7 cells, LeprA720T/T10441 produced a normal basal and maximum activation with a minor increase in the EC50 of leptin. CONCLUSIONS/INTERPRETATION: The data identify two new quantitative trait loci that are responsible for a major part of obesity and hyperinsulinaemia as produced by recessive genes in NZO mice. LeprA720T/T1044I alone cannot produce obesity, but may enhance the effects of other obesity/insulin resistance genes in this mouse model.

Adipose Tissue↗
PubMed1997

Anti-obesity effect of MPV-1743 A III, a novel imidazoline derivative, in genetic obesity.

MPV-1743 A III ((+/-)-4-(5-fluoro-2,3-dihydro-1H-inden-2-yl)-1H-imidazole) is a novel imidazoline derivative. In this study, it was shown to bind with high affinity to alpha2-adrenoceptor subtypes alpha2A (IC50) = 0.66 +/- 0.06 nM), alpha2B (IC50) = 3.8 +/- 0.53 nM), alpha2C (IC50) = 3.1 +/- 0.61 nM) in the recombinant S115 cells and to alpha2D (IC50 = 0.94 +/- 0.10 nM) in the rat submandibular gland. MPV-1743 A III also showed remarkably high affinity to alpha1-adrenoceptors (IC50 = 150 +/- 12 nM) in the rat cerebral cortex and to imidazoline I2b-binding sites (IC50) = 150 +/- 5.0 nM) in the rat liver. The functional alpha2-adrenoceptor antagonistic effect of MPV-1743 A III was demonstrated by studying the ability of orally administered MPV-1743 A III to reverse and prevent the alpha2-adrenoceptor agonist detomidine-induced mydriasis in rat. The anti-obesity effect of MPV-1743 A III was investigated in genetically obese (fa/fa) Zucker rats in two different phases of obesity. Chronic treatment with MPV-1743 A III (0.3 3 mg/kg per day p.o. for 3 weeks) dose dependently decreased weight gain in early-phase obesity. In fully established obesity, GDP binding to mitochondria and expression of uncoupling protein mRNA were increased in brown adipose tissue by MPV-1743 A III indicating an activation of non-shivering thermogenesis. The present study shows that MPV- 1743 A III has a modest anti-obesity effect in the genetic rodent model of obesity. The relative importance of alpha2- and alpha1-adrenoceptors and imidazoline I2b-binding sites in mediating the effects of MPV-1743 A III needs further evaluation.

Adipose Tissue, Brown↗
PubMed2006

Reducing weight increases postural stability in obese and morbid obese men.

OBJECTIVE: To investigate the effect of weight loss on balance control in obese and morbid obese men. METHODS: In a longitudinal and clinical intervention study, postural stability was measured with a force platform before and after weight loss in men. Weight loss was obtained in obese men (mean body mass index (BMI)=33.0 kg/m(2)) by hypocaloric diet until resistance and in morbid obese men (mean BMI=50.5 kg/m(2)) by bariatric surgery. Morbid obese men were tested before surgery, and 3 and 12 months after surgery when they had lost 20 and nearly 50% of initial body weight, respectively. Normal weight individuals (mean BMI=22.7 kg/m(2)) were tested twice within a 6- to 12-month period to serve as control. Body fatness and fat distribution measures, and posturographic parameters of the center of foot pressure (CP) along the antero-posterior and medio-lateral axes for conditions with and without vision were performed in all subjects. RESULTS: Weight loss averaged 12.3 kg after dieting and 71.3 kg after surgery. Body weight remained unchanged in the control group. After weight loss, nearly all measures of postural stability were improved with and without vision (i.e., CP speed and range in antero-posterior and medio-lateral axes). A strong linear relationship was observed between weight loss and improvement in balance control measured from CP speed (adjusted R (2)=0.65, P<0.001). CONCLUSION: Weight loss improves balance control in obese men and the extent of the improvement is directly related to the amount of weight loss. This should decrease the habitual greater risk of falling observed in obese individuals.

Adult↗
PubMed1995

Evidence against either a premature stop codon or the absence of obese gene mRNA in human obesity.

Obese (ob) gene expression in abdominal subcutaneous adipocytes from lean and obese humans was examined. The full coding region of the ob gene was isolated from a human adipocyte cDNA library. Translation of the insert confirmed the reported amino acid sequence. There was no difference in the sequence of an reverse transcription PCR product of the coding region from five lean and five obese subjects. The nonsense mutation in the ob mouse which results in the conversion of arginine 105 to a stop codon was not present in human obesity. In all 10 human cDNAs, arginine 105 was encoded by CGG, consequently two nucleotide substitutions would be required to result in a stop codon. To compare the amount of ob gene expression in lean and obese individuals, radiolabed primer was used in the PCR reaction with beta-actin as a control. There was 72% more ob gene expression (P < 0.01) in eight obese subjects (body mass index, BMI = 42.8 +/- 2.7) compared to eight lean controls (BMI = 22.4 +/- 0.8). Regression analysis indicated a positive correlation between BMI and the amount of ob message (P < 0.005). There was no difference in the amount of beta-actin expression in the two groups. These results provide evidence that ob gene expression is increased in human obesity; furthermore, the mutations present in the mouse ob gene were not detected in the human mRNA population.

Adult↗
PubMed2005

The pharmacokinetics of daptomycin in moderately obese, morbidly obese, and matched nonobese subjects.

Daptomycin pharmacokinetics were studied in adult volunteers who were moderately obese (body mass index [BMI] = 25-39.9 kg/m2) or morbidly obese (BMI > or =40 kg/m2) and a matched (gender, age, renal function) nonobese (BMI between 18.5 and 24.9 kg/m2) control group. All subjects received a dose of 4 mg/kg total body weight (TBW) by intravenous infusion (30 minutes). Daptomycin plasma half-life, the fraction of the dose excreted unchanged in urine, and daptomycin absolute renal clearance (mL/h) were unchanged as a function of obesity. The absolute volume of distribution (Vz and Vss) and plasma clearance (CL) for daptomycin were higher in obese subjects as compared to nonobese matched controls. The rate of change of Vz and CL with increasing BMI was greater when these pharmacokinetic parameters were expressed in absolute terms compared to when they were normalized for TBW or ideal body weight. This suggests that increases in body mass associated with obesity are proportionality higher than the corresponding increases in Vd and CL. Exposure to daptomycin in obese subjects (Cmax, AUC) was increased 25% and 30%, respectively, compared to nonobese matched controls, well within the range that was previously determined to be safe and well tolerated. Daptomycin may be dosed based on total body weight, and no adjustment in daptomycin dose or dose regimen should be required based solely on obesity.

Adult↗
PubMed1997

A comparison of fat intake of normal weight, moderately obese and severely obese subjects.

BACKGROUND: Excess dietary fat has been implicated in the etiology of obesity. METHODS: This study examined the fat intake of three weight groups, normal (20.0 < or = BMI < or = 27.0), moderately obese (27.1 < or = BMI < or = 39.9) and severely obese (BMI > or = 40.0). Each group contained 50 subjects. Detailed 3-day food records were used to gather the nutritional data. Anthropometric and sociodemographic information was also collected. RESULTS: Overall fat intake was 89 +/- 42 g/day or 37 +/- 10% of total energy. Total fat (g/1000 kcalories) intake was found to be significantly higher in the obese groups (p < 0.05). Subjects in the moderately and severely obese groups consumed significantly more fat and cholesterol and less carbohydrate than did normal weight subjects. Compared to the normal weight subjects, obese subjects also had higher intakes of saturated, monounsaturated and polyunsaturated fat (as a percentage of dietary energy). There was no difference in energy or protein intake, and P/S ratio among the three groups. BMI was strongly positively correlated with total fat, saturated, monounsaturated, polyunsaturated fat, cholesterol, and protein intake (as g/day only), and negatively correlated with carbohydrate intake and the CHO/FAT ratio. Energy intake was not significantly associated with BMI. CONCLUSION: A high fat diet may promote obesity, independently of its calorie contribution.

Adult↗
PubMed2005

Report on childhood obesity in China (1)--body mass index reference for screening overweight and obesity in Chinese school-age children.

PURPOSE: To establish and propose a national body mass index (BMI) reference for screening overweight and obesity in Chinese school-age children and adolescents. METHODS: 2000 CNSSCH (Chinese National Survey on Students Constitution and Health) data, including 216 620 primary and secondary school students aged 7 to 18 years old, were used as a reference population. Compared with those of the NCHS international reference, three temporary sets of cut-off BMI were proposed by testing different combinations of P85, P90, and P95. When physiological and biochemical measures between and among "obesity", "overweight", and "normal weight" groups were taken into consideration, set II was selected to be the most appropriate one. The sex-age-specific curves were then plotted and smoothed by using B-spline method. RESULTS: Based on the samples from costal developed metropolis, the BMI curves successfully overcame the shortcomings of lower and level-off tendency of the Chinese total population. Temporary set II, composed by cut-offs of P85 for overweight and P95 for obesity, was finally selected by its sensitivity and peculiarity. BMI 24 and 28 were used as cut-offs for overweight and obesity for both males and females aged 18 years old. These cut-offs, consistent with Chinese Adult's Reference, was proposed as the Body mass index reference for screening overweight and obesity in Chinese school-age children and adolescents. CONCLUSION: The new reference clearly showed its superiorty in both prospectivity and actuality. The proposed reference minimized the gaps of the BMI curve between Chinese adolescents and the international reference. Most importantly was that it was consistent with the Eastern Asia ethnic characteristics of body fatness growth. It was therefore proposed by the Working Group on Obesity in China (WGOC) to use it as an nationwide reference for screening overweight and obesity of school-age children and adolescents in China.

Adolescent↗