There has been an escalating incidence of obesity along with type 2 diabetes mellitus (T2DM), as well as other co-morbidities so much so that the term diabesity had to be coined for this worldwide epidemic. Different attempts have been done to unravel the etiology of this ever-escalating problem, however, there has been a failure to control it. All the newer combinations like Qsymia (topiramate, phentermine), Contrive (naltrexone: bupropion), liraglutide, etc., have been unsuccessful with either cost prohibitions or side effects/contraindications. Thus, attention had shifted to dietary therapies like high protein diet, the mediterranean diet (MD), and Probiotic therapy. However, none has ensured the sustenance of weight reduction. In 2018, we reviewed how the very-low-calorie ketogenic diet (VLCKD) might be successful not only in obesity therapy but also in correlated endocrine dysfunction. Recently, there has been a lot of resurgence of the use of VLCKD. The authors performed an extensive search on various platforms like PubMed; Google scholar; Web of Science; Embase; Cochrane review library utilizing the MeSH terms; “Obesity/Overweight”; “Various diets MD”; “VLCKD to assess the efficacy of which diet is better” from 1995 till date. Nevertheless, it has been seen that the efficacy of this is not seen uniformly. Thus, the group of Muscogiuri G recently observed that compliance with MD acts in the form of the anticipation of the effectiveness of VLCKD, thus the role of MD in obesity persists because of anti-inflammatory along with antioxidant actions of MD that ensures good ketosis generation.
Systematic Review | Volume 6 | Number 1| 1 Copyright 2019 by Kaur KK. This is an open-access article distributed under Creative Commons Attribution 4.0 International License (CC BY 4.0), which allows to copy, redistribute, remix, transform, and reproduce in any medium or format, even commercially, provided the original work is properly cited. cc Article information Received: February 2nd, 2019; Revised: March 13th, 2019; Accepted: March 14th, 2019; Published: March 22nd, 2019 Kulvinder Kochar Kaur, MD1*; Gautam Allahbadia, MD, DNB2; Mandeep Singh, MD, DM3
1Southern Illinois University Nutrition Department, Carbondale, IL, USA; Department of Nutrition, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA, USA (Former Affiliation Universities where part of the USDA/NIFA funded work on sensory nutrition education with exotic fruits and vegetables, was completed) 2Department of Computer Science, Southern Illinois University, Carbondale, Illinois, USA; Kronsys Inc, Raleigh, North Carolina, USA *Corresponding author Srimathi Kannan, PhD (Former Assistant Professor) Department of Nutrition, Southern Illinois University, Carbondale, IL, USA Tel. (413) 230-6847 Fax: 4132306847 E-mail: srimathik@gmail.com
Introduction: N-myristoyltransferase (NMT) is implicated in myristoylation, required for biological activities of several proteins.Its gene N-myristoyltransferase 1 (NMT1) has been found to be overexpressed and hypermethylated in Visceral Adipose Tissue (VAT) of severely obese individuals with Metabolic Syndrome (MetS+) versus without (MetS-).Objective: The aim of this study was to verify the associations between NMT1 gene polymorphisms Single Nucleotide Polymorphisms (SNPs) and metabolic complications among obese subjects.Methods: Associations between SNPs and determinants of MetS were tested with 1752 obese participants undergoing a bariatric surgery.The effect of selected SNPs on methylation, and correlation with expression levels of NMT1 were verified in subgroups.Results: Rs2239921 was significantly associated with systolic (p=0.03) and diastolic (p<0.0001)blood pressures.Rs2239923 was associated with plasma High Density Lipoprotein-Cholesterol or HDL-Cholesterol (HDL-C) levels (p=0.05), while rs2269746 was associated with Low Density Lipoprotein-Cholesterol or LDL-Cholesterol (LDL-C) (p=0.006) and Total-Cholesterol (Total-C) levels (p=0.004).Rs1005136 (p=0.03),rs8066395 (p=0.03) or rs2157840 (p=0.04) were associated with plasma concentrations of C-Reactive Protein (CRP).Phenotype-associated SNPs were associated with NMT1 methylation levels of six CpG sites.NMT1 methylation levels of one CpG site, cg10755730, correlated with gene expression levels (r=0.57;p=0.04).Conclusion: These results suggest that the presence of NMT1 SNPs is associated with altered plasma lipid levels as well as with increased inflammation markers and blood pressure among severely obese patients.
Objective: We tested the hypothesis that visceral adiposity, compared with general adiposity, would explain more of the variance in cardiovascular disease (CVD) risk factors.Research Method and Procedures: Subjects were 464 adolescents (238 black and 205 girls). Adiposity measures included Visceral adipose tissue (VAT; magnetic, resonance imaging), percent body fat (%BF; DXA), BMI, and waist Girth (anthropometry). CVD risk factors were fasting insulin, fibrinogen, total to high-density lipoprotein-cholesterol ratio, triglycerides (TGs), systolic blood pressure, and left ventricular mass indexed to height 2.7.Results: After adjustment for age, race, and sex, all adiposity indices explained significant proportions of the variance in all of the CVD risk factors; %BF tended to explain more variance than VAT. Regression models that included both %BF and VAT found that both indices explained independent proportions of the variance only for total to high-density lipoprotein-cholesterol ratio. For TGs, the model that included both %BF and VAT found that only VAT was significant. For systolic blood pressure and left ventricular 2.7 mass indexed to height, anthropometric measures explained more of the variance than VAT and %BF.Discussion: The hypothesis that visceral adiposity would explain more variance in CVD risk than general adiposity was not supported in this relatively large sample of black and white adolescents. Only for TGs did it seem that VAT was more influential than %BF. Perhaps the deleterious effect of visceral adiposity becomes greater later in life as it increases in proportion to general adiposity.
Objectives: The objectives were to understand how the retirement decisions of older Americans influence household food consumption patterns by gender and, in turn, to examine the impact of the change in food consumption on weight.Research Methods and Procedures: This study used five waves of the Health and Retirement Study (1992 to 2002; n = 28,117). Participants were 50 to 71 years old during the study period. We used longitudinal regression analyses controlling for health events, spousal factors, socioeconomic factors, and individual fixed effects over time.Results: Retirement of the individual and of his/her spouse reduced the individual's monthly spending on eating out by $10 and $7 on average, respectively, but did not change household spending oil food at home. The wife's, but not the husband's, retirement decreased the spouse's spending on eating out by $13/mo. Spending on eating out was a significant but weak (0.003BMI/$) predictor of weight gain.Discussion: The decrease in spending on eating out after retirement, particularly women's, suggests that people eat out less when they have more time for food preparation at home. However. increases in other risks of weight gain with retirement, such as physical inactivity, could counteract the effects of eating out less.
Objective: Reduction of cortisone to cortisol is mediated by 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta HSD1), a putative key enzyme in obesity-related complications. Experimental studies suggest that adipokines, notably leptin and tumor necrosis factor-alpha (TNF-alpha), are of importance for 11 beta HSD1 activity. We hypothesized that the regulation of hepatic preceptor glucocorticoid metabolism is gender-specific and associated with circulating levels of leptin and TNF-a receptors and/or sex hormones.Research Methods and Procedures: A total of 34 males and 38 women (14 premenopausal and 22 postmenopausal) underwent physical examination and fasting blood Sampling. Insulin sensitivity was tested by euglycemic hyperinsulinemic clamps, and hepatic 11 beta HSD1 enzyme activity was estimated by the conversion of orally-ingested cortisone to cortisol.Results: Hepatic 11 beta HSD1 activity was negatively associated with leptin and soluble TNF (sTNF) r1 and sTNFr2 in males. These correlations remained significant after adjustment for age and insulin sensitivity, and for sTNF-alpha receptors also after adjustment of BMI and waist circumference. In contrast, 11 beta reduction of cortisone was positively associated to leptin in females after adjustment for BMI and waist circumference.Discussion: Hepatic 11 beta reduction shows different links to circulating adipocyte-derived hormones in males and females. This emphasizes the need for further studies on tissue-specific regulation of 11 beta HSD1 in both genders.
OBJECTIVE:Human embryonic stem cells (hESCs) have raised great hopes for future clinical applications. Several groups have succeeded in differentiating hESCs into adipocytes, as determined by morphology, mRNA expression, and protein secretion. However, determination of lipolytic response, the most important characteristic of adipocytes, has not been performed. This work was intended to study adipogenic conversion of hESCs by functional assessment of differentiation.RESEARCH METHODS AND PROCEDURES:Single undifferentiated colonies were allowed to transform into embryonic bodies. mRNA expression for a set of adipocyte-specific genes and leptin/adiponectin secretion and lipolysis were assessed at different time-points after differentiation.RESULTS:In contrast to primary human adipocytes, hESC-derived adipocytes showed a very small response to classical beta-adrenergic agonists, although they expressed the major genes in the lipolytic cascade. In contrast, there was a significant lipolytic response to atrial natriuretic peptide.DISCUSSION:Although hESC-derived adipocytes seem to be morphologically and expressionally similar to mature adipocytes, there are important functional differences that could depend on their early developmental origin. We conclude that, in contrast to mature adipocytes, hESC-derived adipocytes display a differential response to atrial natriuretic peptide and catecholamines.
Objective: To review the evidence for and against the role of visceral adipose tissue as a major contributor to the metabolic complications of obesity through abnormal regulation of lipolysis.Research Methods and Procedures: Data from investigators in the field who have studied visceral adiposity and metabolic health and/or regional and systemic free fatty acid (FFA) release were considered.Results: Although visceral fat mass was positively correlated with adverse health consequences and excess FFA availability, visceral fat was not the source of excess systemic FFA availability. Upper body non-visceral fat contributes the majority of FFAs in lean, obese, diabetic, and non-diabetic humans. Increasing amounts of visceral fat probably result in greater hepatic FFA delivery.Discussion: Systemic, as opposed to hepatic, insulin resistance is unlikely to be caused by high rates of visceral adipose tissue lipolysis.
Objective: To assess whether dietary linolenic acid is associated with fasting insulin and glucose.Research Methods and Procedures: In a cross-sectional design, we studied 3993 non-diabetic participants of the National Heart, Lung, and Blood Institute Family Heart Study 25 to 93 years of age. Linolenic acid was assessed through a food frequency questionnaire, and laboratory data were obtained after at least a 12-hour fast. We used generalized linear models to calculate adjusted means of insulin and glucose across quartiles of dietary linolenic acid.Results: From the lowest to the highest sex-specific quartile of dietary linolenic acid, means +/- standard error for logarithmic transformed fasting insulin were 4.06 +/- 0.02 (reference), 4.09 +/- 0.02, 4.13 +/- 0.02, and 4.17 +/- 0.02 pM, respectively (trend, p < 0.0001), after adjustment for age, sex, energy intake, waist-to-hip ratio, smoking, and high-density lipoprotein-cholesterol. When dietary linolenic acid was used as a continuous variable, the multivariable adjusted regression coefficient was 0.42 +/- 0.08. There was no association between dietary linolenic acid and fasting glucose (trend p = 0.82).Discussion: Our data suggest that higher consumption of dietary linolenic acid is associated with higher plasma insulin, but not glucose levels, in non-diabetic subjects. Additional studies are needed to assess whether higher intake of linolenic acid results in an increased insulin secretion and improved glucose use in vivo.
OBJECTIVE:Obesity is a complex multifactorial disease that is often associated with cardiac arrhythmias. Various animal models have been used extensively to study the effects of obesity on physiological functions, but, to our knowledge, no study related to ionic membrane currents has been performed on isolated cardiac myocytes. Therefore, we examined the electrophysiological characteristics of four ionic currents from isolated left ventricular myocytes of a high-energy (HE)-induced obesity rat model.RESEARCH METHODS AND PROCEDURES:Male Sprague-Dawley rats were fed with either a control diet or a diet containing 33% kcal as fat (HE) for 14 weeks starting at 6 weeks of age. Voltage-clamp experiments were performed on ventricular myocytes. Leptin receptor (ObR) expression was measured using ObR enzyme-linked immunosorbent assay.RESULTS:In the HE group, rats designated as obese did not develop a cardiac hypertrophy, either at the organ level or at the cellular level. Densities and kinetics of the L-type calcium current, the transient outward potassium current, the delayed rectifier potassium current, and the sodium-calcium exchange current (I(NCX)) were not significantly different between control and obese rats. A down-regulation of ObR expression was evidenced in the heart of obese rats compared with controls. Acute exposure (5 minutes) of leptin (100 nM) did not induce a significant modification in the current densities either in control or in obese rats, except for I(NCX) density measured in control rats.DISCUSSION:The absence of effect of leptin on I(NCX) in obese rats could be a potential arrhythmogenic substrate in obesity.
OBJECTIVE:Data from rodents provide evidence for a causal role of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) in the development of obesity and its complications. In humans, 11beta-HSD-1 is increased in subcutaneous adipose tissue (SAT) of obese patients, and higher adipose 11beta-HSD-1 was associated with features of the metabolic syndrome. To date, there is no evidence for an increased expression of 11beta-HSD-1 in human visceral adipose tissue (VAT), although VAT is the major predictor for insulin resistance and the metabolic syndrome.RESEARCH METHODS AND PROCEDURES:11beta-HSD-1 and hexose-6-phosphate dehydrogenase (the enzyme responsible for the synthesis of nicotinamide adenine dinucleotide phosphate, the cofactor required for 11beta-HSD-1 oxoreductase activity) mRNA levels were measured using real-time quantitative reverse transcriptase-polymerase chain reaction in abdominal SAT and VAT biopsies obtained from 10 normal-weight and 12 obese women. Adiponectin mRNA was used as an internal control.RESULTS:11beta-HSD-1 mRNA concentrations were significantly increased in both SAT and VAT of obese patients (720% and 450% of controls, respectively; p < 0.05) and correlated with hexose-6-phosphate dehydrogenase mRNA levels. The level of VAT 11beta-HSD-1 mRNA correlated with anthropometric parameters: BMI (r = 0.41, p = 0.05), waist circumference (r = 0.44, p = 0.04), abdominal sagittal diameter (r = 0.51, p = 0.02), and percentage fat (r = 0.51, p = 0.02).DISCUSSION:Our results demonstrate for the first time that 11beta-HSD-1 mRNA expression is increased in VAT from obese patients. They strengthen the importance of 11beta-HSD-1 in human obesity and its associated complications and suggest the need of clinical studies with specific 11beta-HSD-1 inhibitors.
OBJECTIVE:Abnormalities in physicochemical properties of the cell membranes may underlie the defects that are strongly linked to hypertension. Recent evidence indicates that adiponectin may have protective effects against cardiovascular diseases. The purpose of the present study was to assess the possible link between plasma adiponectin and membrane fluidity in normotensive (NT) and hypertensive (HT) men.RESEARCH METHODS AND PROCEDURES:We measured the membrane fluidity (a reciprocal value of membrane microviscosity) of erythrocytes in NT and HT men by using an electron paramagnetic resonance and spin-labeling method.RESULTS:The order parameter (S) for the spin label agent (5-nitroxide stearate) and the peak height ratio (h0/h(-1)) for 16-nitroxide stearate in the electron paramagnetic resonance spectra of erythrocytes were significantly higher in HT men than in NT men, indicating that membrane fluidity of erythrocytes was decreased in HT men compared with NT men. Both of plasma adiponectin and nitric oxide (NO) metabolite levels were significantly lower in HT men than in NT men. The plasma adiponectin levels were correlated with plasma NO metabolites. The S and the h0/h(-1) of erythrocytes were inversely correlated with the plasma adiponectin and NO metabolite levels, indicating that the decreased membrane fluidity of erythrocytes was associated with hypoadiponectinemia and reduced plasma NO metabolites.DISCUSSION:The results of the present study demonstrated that plasma adiponectin levels were lower in HT men than in NT men and that hypoadiponectinemia was associated with decreased membrane fluidity of erythrocytes. The finding suggests that adiponectin may be linked to the rheologic behavior of the erythrocytes and the microcirculation in men, at least in part, by the NO-dependent mechanism.
Objective: To study the relationship between BMI at age 18 years and later attained education, with control for intelligence and parental social position.Research Methods and Procedures: A cohort of 752,283 Swedish men born from 1952 to 1973 were followed in registers with respect to attainment of high education (>= 15 years of education) until December 31, 2001. Intelligence and BMI (kilograms per meter squared) were measured at compulsory military conscription at age 18 years. Ninth grade school marks were available for a subgroup born from 1972 to 1973 (N = 93,374). The hazard ratio for attaining high education was estimated with proportional hazard regression analysis controlling for intelligence, height, parental socioeconomic position, country of birth, conscription center, and municipality.Results: Young men who were obese (BMI ! 30) at age 18 years (N = 10,782) had a much lower chance of attaining a high education than normal-weight subjects [(18.5 <= BMI < 25); adjusted hazard ratio 0.48 (95% confidence interval, 0.45, 0.52)]. Young men who were obese at age 18 had lower mean ninth grade school marks than young men with normal weight at any given intelligence level.Discussion: Obese men in Sweden are doing much worse in the educational system than their normal-weight counterparts even after adjustments for intelligence and parental socioeconomic position. Discrimination in the educational system and other sectors of the society may explain these strong associations.
Childhood obesity is already epidemic in some areas of the world and is on the rise in others ((1)), and lifestyle factors such as poor diet and lack of physical exercise are known contributing causes ((2)). Economic evaluation is an important tool in helping to determine the costs and benefits of interventions and is increasingly used as a resource by decision-makers. The study by Wang et al. ((3)) is to be commended as the first published paper to examine the cost effectiveness of a school-based program to prevent obesity through lifestyle changes. The intervention was delivered through an integrated classroom program focused on reducing television viewing, increasing activity levels, and improving nutrition ((4)). The prevalence of obesity between baseline and follow-up decreased in the intervention group (from 23.6% to 20.3%) for girls, relative to an increase in the control group from 21.5% to 23.7%. There was no statistically significant difference in the change in prevalence of obesity in boys ((4)). The Wang et al. ((3)) economic model linked overweight as a child to overweight as a young adult to overweight in middle age and linked this to mortality, morbidity, and medical costs. The model incorporated the costs of the intervention, quality of life, mortality, and downstream health service costs and productivity associated with obesity ((3)). The authors estimated through their model a cost-per-quality adjusted life year (QALY)11 Nonstandard abbreviations: QALY, quality adjusted life year; CEAC, cost effectiveness acceptability curve. gain of US$4305 for girls (range from sensitivity analysis US$1612 to US$9010) with the model most sensitive to the medical care costs averted and the discount rate. There are four key limitations of the economic modeling. The first and most serious limitation is the lack of evidence concerning children's weight after the 2-year intervention period. The model assumed that weight loss would be retained but did not specify the basis for this assumption. As most obesity intervention trials show some remission of gains achieved post-intervention, this is a surprising assumption. Second, the possibility of relapse is not dealt with in the sensitivity analysis; thus, the reported range does not allow for the likelihood of relapse after trial end. The lack of good quality data linking overweight as a child to overweight as an adult is also a concern. Even where models do exist, whether it is reasonable to apply historic relationships developed when the pattern of overweight and obesity was vastly different to that of today is surely a matter for discussion. Third, the evaluation proceeds based on the results for girls only. There was no statistically significant improvement for boys. The intervention was dominated for boys (more expensive and no gain). While subgroup analysis is useful for hypothesis generation, it represents ex-post data dredging when it does not relate to an a priori expectation and, thus, leads to a greater risk of a chance finding. It also is unlikely that the intervention could be implemented for girls only in the normal co-educational setting; therefore, the economic analysis should have taken pupils as a whole. Last, the model incorporates downstream medical costs of being overweight/obese at age 40 to 65 years. Given that this is 30 to 55 years in the future, the confidence that can be placed in these estimates is low. We note that the authors are very aware of the problems posed by data limitations, as highlighted in their discussion. The issue remains that the conclusion regarding program performance depends on the range of assumed values included in the sensitivity analysis. While the authors suggest these to be conservative, it is not clear that this is the case, especially regarding the assumption that observed gains in obesity prevalence are retained beyond trial end. We have, therefore, performed further modeling to explore the implication of adopting a more conservative set of assumptions using an exact replication of the published model. Alternative assumptions to the four main limitations discussed above lead to possible estimates ranging from US$69 to US$35,860 per QALY (exchange rate March 2006) and demonstrate that the model is sensitive to these parameters ((5)). This provides a different message to policy-makers than the reported $4000 per QALY gained. Critical gaps in the literature, particularly regarding long- term studies into children's outcomes after obesity prevention programs and evidence linking children's weight and adult outcomes, lead to large uncertainty in the estimates of cost effectiveness. This is illustrated by the further analyses we have undertaken. It may not be possible to draw clear conclusions about performance of the intervention. With our more conservative set of assumptions, the intervention no longer appears highly cost effective, especially in the context of a prevention program where funders will need to wait many years for benefits to be realized. The lessons are two-fold. First, the assumptions adopted as the base-case and incorporated into sensitivity analysis are highly critical, and the reasons for their selection need to be clearly specified. We also note the tradition of adopting conservative assumptions, which does not seem to have been followed in this case. Second, economic evaluations need to highlight uncertainties and point to priorities for future research to enable evidenced-based estimates of performance to be derived. Not only should sensitivity analysis be performed, but the reason for selecting the parameter values should be explained. Preferably a stochastic/probabilistic analysis should be performed (generated either through Monte Carlo simulation or bootstrapping) which allows the derivation of cost effectiveness acceptability curves (CEACs) ((6)). CEACs represent uncertainty by providing decision-makers with the probability that an intervention is cost effective given a specific funding threshold. In addition, expected value of information analysis can provide a guide as to which additional research information will be most valuable to inform policy decisions ((6)). The area of childhood obesity poses many challenges for researchers. There is a great need for quality economic evaluation alongside the growing body of primary research. It is critical that economic evaluation is based on realistic assumptions and that it provides decision-makers with a thorough analysis of uncertainty. Quality evaluations will also provide valuable information to guide future research activities. Careful and insightful evaluation in this area is critical, as there are potentially large benefits from childhood interventions that are so far unidentified through quality research.
OBJECTIVE:To investigate the effects of surgically induced weight loss on exercise capacity in patients with morbid obesity (MO).RESEARCH METHODS AND PROCEDURES:A prospective 1-year follow-up study was carried out, with patients being their own controls. A symptom-limited cardiopulmonary exercise stress test was performed in 31 MO patients (BMI > 40 kg/m2) before and 1 year after undergoing bariatric surgery.RESULTS:At 1 year after surgery, weight was reduced from 146 +/- 33 to 95 +/- 19 kg (p < 0.001), and BMI went from 51 +/- 4 to 33 +/- 6 kg/m2 (p < 0.001). After weight loss, obese patients performed each workload with lower oxygen consumption, heart rate, systolic arterial pressure, and ventilatory volume (p < 0.001). This reduced energy expenditure allowed them to increase the duration of their effort test from 13.8 +/- 3.8 to 21 +/- 4.2 minutes (p < 0.001). Upon finishing the exercise, MO patients before surgery were able to reach only 83% of their age-predicted maximal heart rate, and their respiratory exchange ratio was 0.87 +/- 0.06. After weight loss, those values were 90% and 1 +/- 0.08, respectively (p < 0.01). When we compared the peak O2 pulse corrected by fat free mass before and after surgery, no significant differences between the groups were found.DISCUSSION:After surgically induced weight loss, MO patients markedly improved their exercise capacity. This is due to the fact that they were able to perform the external work with lower energy expenditure and also to increase cardiovascular stress, optimizing the use of cardiac reserve. There were no differences in cardiac function before and after surgery.
OBJECTIVE:To determine the effect of short-term weight loss in obese women on concentrations of plasma cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP), two new risk factors for cardiovascular disease.RESEARCH METHODS AND PROCEDURES:Plasma CETP and PLTP mass concentrations were measured in 38 obese, non-diabetic women before and after a moderate, 4% weight loss that was obtained by a 1250 kcal/d diet for 4 weeks. Anthropometric and biological parameters were measured before and after weight loss.RESULTS:Plasma CETP concentration decreased substantially after weight loss (2.76 +/- 0.79 before and 2.31 +/- 0.69 mg/L after; p = 0.000), and the same was true for plasma PLTP concentration (9.01 +/- 2.44 mg/L before vs. 8.34 +/- 2.57 after; p = 0.043). The HDL profile shifted toward the small-sized range, with significant decreases in the relative abundance of HDL(2b) and HDL(2a) at the expense of HDL(3b) after weight loss. A significant, positive correlation between CETP and PLTP mass concentrations is reported for the first time in obese patients (r = 0.43, p = 0.004), and weight reduction was accompanied by early, concomitant, and parallel decreases in plasma CETP and PLTP levels (r = 0.47, p = 0.003). The significant relationship between CETP and PLTP levels was lost after the dietary intervention (r = 0.27; p = 0.11).DISCUSSION:CETP and PLTP correlate positively and significantly in obese patients. The hypocaloric dietary manipulation constitutes a relevant intervention to reduce rapidly and simultaneously plasma levels of CETP and PLTP. The impact of reduced PLTP activity on HDL size appeared to be more prominent than the impact of concomitant reduction in CETP activity.
OBJECTIVE:To assess the efficacy of a Web-based tailored behavioral weight management program compared with Web-based information-only weight management materials.RESEARCH METHODS AND PROCEDURES:Participants, 2862 eligible overweight and obese (BMI = 27 to 40 kg/m2) members from four regions of Kaiser Permanente's integrated health care delivery system, were randomized to receive either a tailored expert system or information-only Web-based weight management materials. Weight change and program satisfaction were assessed by self-report through an Internet-based survey at 3- and 6-month follow-up periods.RESULTS:Significantly greater weight loss at follow-up was found among participants assigned to the tailored expert system than among those assigned to the information-only condition. Subjects in the tailored expert system lost a mean of 3 +/- 0.3% of their baseline weight, whereas subjects in the information-only condition lost a mean of 1.2 +/- 0.4% (p < 0.0004). Participants were also more likely to report that the tailored expert system was personally relevant, helpful, and easy to understand. Notably, 36% of enrollees were African-American, with enrollment rates higher than the general proportion of African Americans in any of the study regions.DISCUSSION:The results of this large, randomized control trial show the potential benefit of the Web-based tailored expert system for weight management compared with a Web-based information-only weight management program.
Objective: Our objective was to delineate the potential role of adipogenesis in insulin resistance and type 2 diabetes. Obesity is characterized by an increase in adipose tissue mass resulting from enlargement of existing fat cells (hypertrophy) and/or from increased number of adipocytes (hyperplasia). The inability of the adipose tissue to recruit new fat cells may cause ectopic fat deposition and insulin resistance.Research Methods and Procedures: We examined the expression of candidate genes involved in adipocyte proliferation and/or differentiation [CCAAT/enhancer-binding protein (C/EBP) alpha, C/EBP delta, GATA domain-binding protein 3 (GATA3), C/EBP beta, peroxisome proliferator-activated receptor (PPAR) gamma 2, signal transducer and activator of transcription 5A (STAT5A), Wnt-10b, tumor necrosis factor alpha, sterol regulatory element-binding protein 1c (SREBP1c), 11 beta-hydroxysteroid dehydrogenase, PPARG angiopoietin-related protein (PGAR), insulin-like growth factor 1, PPAR gamma coactivator 1 alpha, PPAR gamma coactivator 1 beta, and PPAR delta] in subcutaneous adipose tissue from 42 obese individuals with type 2 diabetes and 25 non-diabetic subjects matched for age and obesity.Results: Insulin sensitivity was measured by a 3-hour 80 mU/m(2) per minute hyperinsulinemic glucose clamp (100 mg/dL). As expected, subjects with type 2 diabetes had lower glucose disposal (4.9 +/- 1.9 vs. 7.5 +/- 2.8 mg/min per kilogram fat-free mass; p < 0.001) and larger fat cells (0.90 +/- 0.26 vs. 0.78 +/- 0.17 mu m; p = 0.04) as compared with obese control subjects. Three genes (SREBP1c, p < 0.01; STAT5A, p = 0.02; and PPAR gamma 2, p = 0.02) had significantly lower expression in obese type 2 diabetics, whereas C/EBP beta only tended to be lower (p = 0.07).Discussion: This cross-sectional study supports the hypothesis that impaired expression of adipogenic genes may result in impaired adipogenesis, potentially leading to larger fat cells in subcutaneous adipose tissue and insulin resistance.
