Lean Persons Research Articles

The mediating role of internalized weight stigma on weight perception and depression among emerging adults: Exploring moderation by weight and race

The current study examined internalized weight stigma as a mediator of the association between self-perceived weight and depressive symptoms. University students (N = 317) aged 18–25 years completed measures of self-perceived weight, internalized stigma, and depressive symptoms. Multigroup path analyses were used to examine the indirect effect of self-perceived weight on depression through self-stigma. Findings revealed that among persons of size, internalized stigma mediated the effect of higher self-perceived weight on higher depressive symptoms. Among lean persons, this indirect effect was only significant for Black participants. Among all groups, the direct effect of self-perceived weight on internalized stigma was significant. While the present results warrant future replication, the findings expand our understanding of the association between self-perceived weight and depression. These results also illuminate potential future opportunities for rich, culturally informed research and clinical advances that take into account the detrimental role of weight stigma.

Weight Loss Maintenance: Have We Missed the Brain?

Even though obese individuals often succeed with weight loss, long-term weight loss maintenance remains elusive. Dietary, lifestyle and psychosocial correlates of weight loss maintenance have been researched, yet the nature of maintenance is still poorly understood. Studying the neural processing of weight loss maintainers may provide a much-needed insight towards sustained obesity management. In this narrative review, we evaluate and critically discuss available evidence regarding the food-related neural responses of weight loss maintainers, as opposed to those of obese or lean persons. While research is still ongoing, available data indicate that following weight loss, maintainers exhibit persistent reward related feeling over food, similar to that of obese persons. However, unlike in obese persons, in maintainers, reward-related brain activity appears to be counteracted by subsequently heightened inhibition. These findings suggest that post-dieting, maintainers acquire a certain level of cognitive control which possibly protects them from weight regaining. The prefrontal cortex, as well as the limbic system, encompass key regions of interest for weight loss maintenance, and their contributions to long term successful weight loss should be further explored. Future possibilities and supportive theories are discussed.

Natural Killer Cells from the Subcutaneous Adipose Tissue Underexpress the NKp30 and NKp44 in Obese Persons and Are Less Active against Major Histocompatibility Complex Class I Non-Expressing Neoplastic Cells.

There are many types of leukocytes reside in subcutaneous adipose tissue (SAT), and among them, natural killer cells (NKs) comprise a major part. We show that the NKs that reside in the SAT (adipose tissue-derived NK cells; ADNKs) of the abdominal region found with phenotypic differences from the NKs circulating in the peripheral blood derived NK cells (PBNKs). In this survey, flow cytometry phenotyping was used to study the differences between the natural cytotoxicity receptor expression on ADNKs and PBNKs of both obese and lean persons. Also, their cytotoxicity and cytokine production patterns were evaluated. The activation experiments on isolated and expanded NKs with IL-2, IL-15, and IL-21 cytokines revealed the main population of the CD56dim within the total ADNKs of obese persons has an under-expression of NKp30 and NKp44 despite the unchanged levels of NKG2D. The data suggest the suppressive condition of the adipose tissue niche on the NKs response against sensitive major histocompatibility complex class I non-expressing neoplastic cells. As the NKs are the first line of the body’s defense vs tumor formation, this change may lead to the development of transformed cells into the tumors.

Automatic Ingestion Monitoring Device for Diet Control

Food ingestion is the process of intake of food by human beings through their mouth. The present study mainly focused on maintaining ingestion limit for the intake of food for obese person and intake of extra food for lean person. At every intake of food the device will be enabled and the ingestion is maintained by monitoring the jaw movements using EMG and MEMS sensors. Anorexia nervosa, bulimia nervosa and binge eating are the most common eating disorders that are resistant to most drugs treatment and causes serious physical and mental disorders can be identified by this study. Current methodologies used for food intake analysis largely rely on laboratory studies rather than objective observations. The doubly-labeled water is the most accurate method used to calculate the energy consumed over a period of several days. However, it is not capable of identifying individual for the entire episodes. Thus, new approaches for objective and accurate assessment for free living patterns are necessary for monitoring of eating behaviors. The working principles of hardware device and monitoring can be controlled by both manually and by using LABVIEW software. The data could be transmitting using ZIGBEE software to PC and the details can be viewed on the monitor.

Association between pulse pressure and body mass index in hypertensive and normotensive populations in the Korea National Health and Nutrition Examination Survey V, 2010-2012.

The authors conducted a national cross-sectional cohort study to evaluate the associations between pulse pressure (PP) and body mass index (BMI) and sex, according to blood pressure (BP) status. A total of 18812 patients without a history of antihypertensive medication and cardiovascular disease were selected. There was good concordance between PP and the selected cardiovascular risk factors. PP increased with high BMI among patients with normal BP, but decreased with high BMI among patients with hypertension (HTN). BMI (ß, -0.260; SE, 0.039 [P<.001]) and male sex (ß, -4.727; SE, 1.100 [P<.001]) were negatively correlated with PP in a multivariate model adjusted for several risk factors in patients with HTN. In conclusion, PP was negatively correlated with BMI in patients with HTN, which may explain the higher cardiovascular risk in lean persons and women with HTN.

Lean, but not healthy: the 'metabolically obese, normal-weight' phenotype.

Obesity is commonly associated with metabolic dysfunction but there are obese persons who are metabolically healthy. On the opposite side of the coin, there are lean persons who carry multiple cardiometabolic risk factors, typically referred to as metabolically obese, normal-weight (MONW). This has called into question our understanding of obesity and metabolic dysfunction, as an appearance of normal weight may mask significant comorbidities and delay health interventions. High heterogeneity in MONW prevalence rates has been observed, with estimates ranging from as low as 5% to as high as 45%. Reasons for this include sample size effects, differences in MONW definition, social and demographic factors, as well as assumptions made in establishing normal weight. MONW study participants are often characterized by excess visceral adipose tissue and ectopic fat deposition, adipose tissue inflammation, altered inflammatory and adipokine profiles, reduced skeletal muscle mass and low cardiorespiratory fitness. However, more often than not, groups of MONW study participants have been somewhat 'fatter' than the control groups of metabolically healthy lean study participants, which in itself could be responsible for some of the observed differences. Very limited data are available regarding interventions to improve metabolic function in MONW study participants. There is a need for more research to better understand the characteristics of the MONW phenotype, the cause of metabolic dysfunction in the absence of obesity, and evaluate potential therapies so as to facilitate the establishment of clinical guidelines.

Monocyte subsets in blood correlate with obesity related response of macrophages to biomaterials invitro.

Macrophages play a key role in the foreign body response. In this study it was investigated whether obesity affects the acute response of macrophages to biomaterials invitro and whether this response is associated with biomarkers in blood. CD14+monocytes were isolated from blood from obese and age and gender matched lean persons. Monocyte subsets were determined based on CD14 and CD16 on their surface. C-reactive protein (CRP) was measured in peripheral blood. The response of monocyte-derived macrophages to polypropylene (PP), polylactic acid (PLA), polyethylene terephthalate (PET) monofilament, and PET-multifilament (mPET) in culture was based on cytokine production. More IL-6 (for PET), less CCL18 (all materials) and IL-1ra (for PLA) was produced by macrophages from obese patients than lean subjects. Body mass index, serum CRP and to a lesser extend percentages of monocyte subtypes correlated with IL-6, TNFα, CCL18, and IL-1ra production. Taken together, monocyte-derived macrophages of obese patients respond more pro-inflammatory and less anti-inflammatory to biomaterials than macrophages from lean subjects, depending on the material. These results are a step towards personalized medicine for the development of a model or even a blood test to decide which biomaterial might be suitable for each patient.

Plasma Proteins Modified by Advanced Glycation End Products (AGEs) Reveal Site-specific Susceptibilities to Glycemic Control in Patients with Type 2 Diabetes

Protein glycation refers to the reversible reaction between aldoses (or ketoses) and amino groups yielding relatively stable Amadori (or Heyns) products. Consecutive oxidative cleavage reactions of these products or the reaction of amino groups with other reactive substances (e.g. α-dicarbonyls) yield advanced glycation end products (AGEs) that can alter the structures and functions of proteins. AGEs have been identified in all organisms, and their contents appear to rise with some diseases, such as diabetes and obesity. Here, we report a pilot study using highly sensitive and specific proteomics approach to identify and quantify AGE modification sites in plasma proteins by reversed phase HPLC mass spectrometry in tryptic plasma digests. In total, 19 AGE modification sites corresponding to 11 proteins were identified in patients with type 2 diabetes mellitus under poor glycemic control. The modification degrees of 15 modification sites did not differ among cohorts of normoglycemic lean or obese and type 2 diabetes mellitus patients under good and poor glycemic control. The contents of two amide-AGEs in human serum albumin and apolipoprotein A-II were significantly higher in patients with poor glycemic control, although the plasma levels of both proteins were similar among all plasma samples. These two modification sites might be useful to predict long term, AGE-related complications in diabetic patients, such as impaired vision, increased arterial stiffness, or decreased kidney function.

The Obesity Paradox and Heart Failure: A Systematic Review of a Decade of Evidence.

There is scientific consensus that obesity increases the risk of cardiovascular diseases, including heart failure. However, among persons who already have heart failure, outcomes seem to be better in obese persons as compared with lean persons: this has been termed the obesity paradox, the mechanisms of which remain unclear. This study systematically reviewed the evidence of the relationship between heart failure mortality (and survival) and weight status. Search of the PubMed/MEDLINE and EMBASE databases was done according to the PRISMA protocol. The initial search identified 9879 potentially relevant papers, out of which ten studies met the inclusion criteria. One study was a randomized clinical trial and 9 were observational cohort studies: 6 prospective and 3 retrospective studies. All studies used the BMI, WC, or TSF as measure of body fatness and NYHA Classification of Heart Failure and had single outcomes, death, as study endpoint. All studies included in review were longitudinal studies. All ten studies reported improved outcomes for obese heart failure patients as compared with their normal weight counterparts; worse prognosis was demonstrated for extreme obesity (BMI > 40 kg/m2). The findings of this review will be of significance in informing the practice of asking obese persons with heart failure to lose weight. However, any such recommendation on weight loss must be consequent upon more conclusive evidence on the mechanisms of the obesity paradox in heart failure and exclusion of collider bias.

Microalbuminuria and adiponectin in obese nondiabetic nonhypertensive people

Introduction The prevalence of obesity has increased dramatically over the last decade. The first sign of renal injury is microalbuminuria or frank proteinuria. The prevalence of microalbuminuria was positively increased with the increasing waist-to-hip ratio in nonhypertensive individuals. Adiponectin plays a role in the suppression of metabolic derangements that may result in diabetes, obesity, and nonalcoholic fatty liver disease and an independent risk factor for metabolic syndrome. Aim The aim of the study was to evaluate the relationship between obesity, adiponectin level, and microalbuminuria in obese nondiabetic nonhypertensive individuals. Patients and methods This study included 70 individuals who were divided into two groups according to their BMI: the obese group (group I), which included 50 people with BMI at least 30 kg/m2, and the control group (group II), which included 20 lean persons with BMI from 18.5 to 24.9 kg/m2. The study excluded patients with diabetes, hypertension, and chronic kidney disease. The following laboratory investigations were carried out on all subjects: serum glucose level, kidney function tests, and serum adiponectin level. Spot urine samples were collected for complete urinanalysis and tested for microalbuminuria and albumin/creatinine ratio (ACR). Results ACR showed significant increase in the obese group than in the nonobese group, but serum adiponectin showed significantly lower level in the obese group than in the nonobese group. Within the obese group a significant positive correlation was found between ACR and BMI and waist-to-hip ratio, whereas a significant negative correlation was found between ACR and serum adiponectin. Also, within the obese group a significant negative correlation was found between serum adiponectin level and ACR and BMI. Discussion and conclusion Through this study we have confirmed the association of microalbuminuria, obesity, and serum adiponectin. Our study supports the hypothesis that obesity is associated with microalbuminuria in obese people free from diabetes, hypertension, and chronic kidney disease.

Time course of postprandial hepatic phosphorus metabolites in lean, obese, and type 2 diabetes patients

Impaired energy metabolism is a possible mechanism that contributes to insulin resistance and ectopic fat storage. We examined whether meal ingestion differently affects hepatic phosphorus metabolites in insulin-sensitive and insulin-resistant humans. Young, lean, insulin-sensitive humans (CONs) [mean ± SD body mass index (BMI; in kg/m(2)): 23.2 ± 1.5]; insulin-resistant, glucose-tolerant, obese humans (OBEs) (BMI: 34.3 ± 1.7); and type 2 diabetes patients (T2Ds) (BMI: 32.0 ± 2.4) were studied (n = 10/group). T2Ds (61 ± 7 y old) were older (P < 0.001) than were OBEs (31 ± 7 y old) and CONs (28 ± 3 y old). We quantified hepatic γATP, inorganic phosphate (Pi), and the fat content [hepatocellular lipids (HCLs)] with the use of (31)P/(1)H magnetic resonance spectroscopy before and at 160 and 240 min after a high-caloric mixed meal. In a subset of volunteers, we measured the skeletal muscle oxidative capacity with the use of high-resolution respirometry. Whole-body insulin sensitivity (M value) was assessed with the use of hyperinsulinemic-euglycemic clamps. OBEs and T2Ds were similarly insulin resistant (M value: 3.5 ± 1.4 and 1.9 ± 2.5 mg · kg(-1) · min(-1), respectively; P = 0.9) and had 12-fold (P = 0.01) and 17-fold (P = 0.002) higher HCLs, respectively, than those of lean persons. Despite comparable fasting hepatic γATP concentrations, the maximum postprandial increase of γATP was 6-fold higher in OBEs (0.7 ± 0.2 mmol/L; P = 0.03) but only tended to be higher in T2Ds (0.6 ± 0.2 mmol/L; P = 0.09) than in CONs (0.1 ± 0.1 mmol/L). However, in the fasted state, muscle complex I activity was 53% lower (P = 0.01) in T2Ds but not in OBEs (P = 0.15) than in CONs. Young, obese, nondiabetic humans exhibit augmented postprandial hepatic energy metabolism, whereas elderly T2Ds have impaired fasting muscle energy metabolism. These findings support the concept of a differential and tissue-specific regulation of energy metabolism, which can occur independently of insulin resistance. This trial was registered at clinicaltrials.gov as NCT01229059.

You Lose Some, You Win Some: Weight Loss Induces Microbiota and Metabolite Shifts

Obesity is an increasing problem worldwide. Nearly 30% of the world's population is overweight or obese, and this number is on the rise (Ng et al., 2014). Because high body-mass index is a strong risk factor for chronic conditions such as cardiovascular disease and diabetes, and is associated with increased mortality, the growing obesity rates are expected to have a significant impact on quality and expected length of life in the future (Prospective Studies Collaboration, 2009). Although obesity could simply be viewed as an imbalance between caloric intake and metabolism, work in the past decade has revealed an important role of the gut microbiota – the microbial communities present in our intestinal tract – in obesity as well (Turnbaugh et al., 2009). Gut microbes can extract calories from food that we humans cannot digest ourselves, and the composition of the gut microbiota from lean individuals has been shown to be distinct from that of obese persons (Ley, 2010). In addition, stool microbiota from human twin pairs discordant for obesity could transmit the obese phenotype to germ-free mice, suggesting that the gut microbiota plays an active role in obesity (Ridaura et al., 2013).

Obesity, the deadly quartet and the contribution of the neglected daily organ rest - a new dimension of un-health and its prevention.

The "deadly quartet": excessive weight, hypertension, impaired glucose homeostasis, and atherogenic dyslipidemia constitute a greater threat to health than the added effects of smoking and alcohol abuse. It is strongly associated with unrestricted consumption of processed, refined foods. Recent observations from experience in South East Asia shows that the interval between lifestyle changes and associated change in disease pattern is shorter than earlier believed. Recent experience from obesity studies in Africa demonstrates not only dramatic changes in health but also large social consequences from being overweight. Obesity is not only a result of overeating - dozens of other factors are known to contribute. Our palaeolithic forefathers and those living a similar lifestyle today are reported to rarely have diseases and to live a long life. One such group is the Hunzas, living in Northern Pakistan, are reported to live on a daily 1,800-calorie 99% plant-based diet, consisting in 73% of mostly unrefined/unprocessed carbohydrates, 17% fat and 10% protein. They, and most likely also our forefathers, do/did most likely only eat twice a day, at noon and early evening. Calorie-restriction (CR) and also fasting was early recommended and has been so during thousands of years - early Greek medicine and giants such as Hippocrates, Galenus and later also Paracelsus prescribed restrictions in eating and fasting. So did Middle Age physicians and other nutrition experts such as Louis Cornado. Today it is again practiced around the World. Overeating and heavy postprandial metabolism is a great burden to the body causing elevated levels in blood of endotoxin, increased inflammatory and oxidative stress, release of tumor necrosis factor-α, and other pro-inflammatory cytokines, increases in numbers of and activating of leukocytes, a reaction that is potentiated by the presence of large-chain fatty acids and sugars. Various metabolic, uremic, microbiota-derived and environmental poisons accumulate in large amounts in the adipose tissues. High levels of poisons in the adipose tissues decreases the turnover of fats in order to protect other organs. The content in adipose of POPs - altogether 17 dioxins/furans and 18 polychlorinated biphenyl congeners, has been reported to be 2-3 times higher in obese compared to lean persons. Daily fasting consisting in 16 to 18 hours of avoidance of calorie intake offers an interesting alternative. An attractive policy is to abstain from eating between 18:00 in the evening and 10:00 or 12:00 AM, a plan, which I personally have practiced during many years.

Irisin plasma concentration in PCOS and healthy subjects is related to body fat content and android fat distribution

Irisin (Ir), a recently identified adipo-myokine, cleaved and secreted from the protein FNDC5 in response to physical activity, has been postulated to induce the differentiation of a subset of white adipocytes into brown fat and to mediate the beneficial effects on metabolic homeostasis. Metabolic syndrome (MS), a cluster of factors leading to impaired energy homeostasis, affects a significant proportion of subjects suffering from polycystic ovary syndrome (PCOS). The aim of our study was to investigate the relationship between Ir plasma concentrations and metabolic disturbances. The study group consisted of 179 PCOS patients and a population of 122 healthy controls (both groups aged 25–35 years). A subset of 90 subjects with MS was isolated. A positive association between Ir plasma level and MS in the whole group and in controls was found. In subjects with high adipose body content (>40%), Ir was higher than in lean persons (<30%). Our results showed a significant positive association between Ir concentration and android type of adipose tissue in the whole study group and in the control group. Understanding the role of Ir in increased energy expenditure may lead to the development of new therapeutics for obesity and obesity-related diseases.

OBESITY PHENOTYPES IN URBAN MIDDLE-CLASS COHORTS; THE PRIT-LINDAVISTA MERGING EVIDENCE IN MEXICO: THE OPUS PRIME STUDY.

even though overweight and obesity (O/O) are stated diseases, there is still a claim for a so-called "healthy obese" phenotype. Only few reports have explored the presence of different metabolic phenotypes along the body mass index (BMI) range and their corresponding associations to cardiovascular risks. as of BMI, and according to the presence of metabolic syndrome (MS) features (waist circumference, blood pressure, fasting glycemia, and lipid profile), phenotypes were determined. Cardiovascular risk was estimated with atherogenic quotients: total cholesterol/ HDL-c, LDL-c/HDL-c and the triglycerides (TG)/HDL-c index. in 8 405 mexican adults, 36% lean, 43% overweighed and 21% obese, nine phenotypes were identified: for each weight category there were subjects with normal metabolism (none MS factors), intermediate (≤ 2) and dysmetabolic (≥ 3). Only 10.8% of O/O had normal metabolism, and 5.8% of the lean persons were dysmetabolic. Atherogenic risk was higher in dysmetabolic obese persons, but the risk was high among all dysmetabolic people, independently of the weight status. TG/HDL-c showed the same trend. elevated cardiometabolic risk derives from the high prevalence of O/O. A great proportion of non-obese people have intermediate dysmetabolism. A genetic predisposition to obesity, insulin resistance, diabetes and dyslipidemia in Mexican population is blended to an unhealthy lifestyle, yielding to a catastrophic epidemic of diabetes, and cardiovascular diseases.

Adaptation of Hepatic Mitochondrial Function in Humans with Non-Alcoholic Fatty Liver Is Lost in Steatohepatitis

The association of hepatic mitochondrial function with insulin resistance and non-alcoholic fatty liver (NAFL) or steatohepatitis (NASH) remains unclear. This study applied high-resolution respirometry to directly quantify mitochondrial respiration in liver biopsies of obese insulin-resistant humans without (n= 18) or with (n= 16) histologically proven NAFL or with NASH (n= 7) compared to lean individuals (n= 12). Despite similar mitochondrial content, obesehumans with or without NAFL had 4.3- to 5.0-fold higher maximal respiration rates in isolated mitochondria than lean persons. NASH patients featured higher mitochondrial mass, but 31%-40% lower maximal respiration, which associated with greater hepatic insulin resistance, mitochondrial uncoupling, and leaking activity. In NASH, augmented hepatic oxidative stress (H2O2, lipid peroxides) andoxidative DNAdamage (8-OH-deoxyguanosine) was paralleled by reduced anti-oxidant defense capacity and increased inflammatory response. These data suggest adaptation of the liver ("hepatic mitochondrial flexibility") at early stages of obesity-related insulin resistance, which is subsequently lost in NASH.

Paradoxical Associations of Insulin Resistance With Total and Cardiovascular Mortality in Humans.

Insulin resistance is linked to many human chronic diseases. Paradoxically, however, impaired insulin signaling contributes to longevity in various organisms and is suggested as an adaptive mechanism against external stressors, including obesity. We formulated a novel hypothesis that insulin resistance can be beneficial in obese humans, insofar as it does not cause glucose dysmetabolism. N = 5,241 participants aged ≥40 with normal fasting glucose were combined across the 1988-1994 and 1999-2004 National Health and Nutrition Examination Survey datasets. Mean follow-up period was 6.6 years. Insulin resistance was measured with homeostasis model assessment (HOMA-IR). Outcomes were all causes (n = 724), cardiovascular diseases (CVD, n = 316), and cancer mortality (n = 190). Supporting the hypothesis, obese persons with high HOMA-IR showed a decreased risk of total and CVD mortality compared to those with the lowest HOMA-IR. Adjusted hazard ratios were 1.0, 0.8, 0.4, and 0.4 (p(trend) = .02) for all death and 1.0, 0.6, 0.2, and 0.2 (p(trend) < .01) for CVD death. On the other hand, lean persons with high HOMA-IR showed about twice the total and CVD mortality compared to persons with the lowest HOMA-IR (p(trend) < .01, respectively). Insulin resistance in obese individuals may begin as an adaptive mechanism and can be beneficial if it is not associated with glucose dysmetabolism. In contrast, insulin resistance in lean individuals associated with higher risk of total and CVD mortality. Insulin resistance may be multifaceted and conventional approaches to regard insulin resistance itself as a pathological condition may be reconsidered in this light.

The association between leptin and depressive symptoms is modulated by abdominal adiposity.

Evidence for a role of leptin in depression is limited and conflicting. Inconclusive findings may be explained by the complex effect of obesity on leptin signaling. In particular, both hyperleptinemia due to leptin resistance in obese persons as well as low leptin in lean persons can imply that low leptin biological signaling is associated with an increased risk of significant depressive symptoms. We tested whether the relationship between leptin and depressive symptoms is modulated by abdominal adiposity in two population-based studies. Data were from 851 participants (65-94 years) of the InCHIANTI Study and 1064 (26-93 years) of the Baltimore Longitudinal Study of Aging (BLSA). Plasma concentrations of leptin, waist circumference and depressive symptoms via the Center for Epidemiological Studies-Depression scale (CES-D) were assessed. In longitudinal InCHIANTI analyses onset of depressed mood (CES-D≥20) was evaluated over a 9-year follow-up. In pooled cross-sectional analyses the interaction between leptin and waist circumference was significantly associated with CES-D scores ((log)leptin-by-waist interaction p=0.01). Also in longitudinal analyses, the (log)leptin-by-waist interaction term significantly (p=0.04) predicted depressed mood onset over time; depressed mood risk was especially increased for high levels of both leptin and waist circumference. The present findings suggest that low leptin signaling rather than low leptin concentration is a risk factor for depression. Future studies should develop proxy measures of leptin signaling by combining information on abdominal adiposity and leptin level to be used for clinical and research applications.

Munc18c in Adipose Tissue Is Downregulated in Obesity and Is Associated with Insulin

ObjectiveMunc18c is associated with glucose metabolism and could play a relevant role in obesity. However, little is known about the regulation of Munc18c expression. We analyzed Munc18c gene expression in human visceral (VAT) and subcutaneous (SAT) adipose tissue and its relationship with obesity and insulin.Materials and MethodsWe evaluated 70 subjects distributed in 12 non-obese lean subjects, 23 overweight subjects, 12 obese subjects and 23 nondiabetic morbidly obese patients (11 with low insulin resistance and 12 with high insulin resistance).ResultsThe lean, overweight and obese persons had a greater Munc18c gene expression in adipose tissue than the morbidly obese patients (p<0.001). VAT Munc18c gene expression was predicted by the body mass index (B = −0.001, p = 0.009). In SAT, no associations were found by different multiple regression analysis models. SAT Munc18c gene expression was the main determinant of the improvement in the HOMA-IR index 15 days after bariatric surgery (B = −2148.4, p = 0.038). SAT explant cultures showed that insulin produced a significant down-regulation of Munc18c gene expression (p = 0.048). This decrease was also obtained when explants were incubated with liver X receptor alpha (LXRα) agonist, either without (p = 0.038) or with insulin (p = 0.050). However, Munc18c gene expression was not affected when explants were incubated with insulin plus a sterol regulatory element-binding protein-1c (SREBP-1c) inhibitor (p = 0.504).ConclusionsMunc18c gene expression in human adipose tissue is down-regulated in morbid obesity. Insulin may have an effect on the Munc18c expression, probably through LXRα and SREBP-1c.

The Stigma of Obesity Surgery: Negative Evaluations Based on Weight Loss History

The present study investigated the stigma of obesity surgery by examining whether attitudes towards a lean person can change after learning that the person used to be obese but recently lost weight either through surgery or through diet and exercise. Participants (total N = 135) initially viewed an image of a lean woman or man and rated their impression of that individual on a variety of characteristics. Participants were then shown an image of the individual before she/he lost weight and were informed that the weight loss was achieved through surgery or through diet and exercise. Participants once again rated their impressions of that individual. After learning about the previous weight loss, participants rated the individual who lost weight through surgery as significantly more lazy and sloppy, less competent and sociable, less attractive, and having less healthy eating habits. The individual who lost weight through diet and exercise, in contrast, was not evaluated as harshly. Mediation analysis further showed that the difference between the two weight loss conditions in ratings of laziness, competence, and sociability was due to participants viewing surgery patients as less responsible for their weight loss. These findings suggest that learning about someone's weight history can negatively impact the way that person is seen by others. Furthermore, these findings suggest that the stigma may be strongest for people who lose weight through obesity surgery because those individuals are not seen as being responsible for their weight loss.