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1.  Depot-specific Regulation of the Conversion of Cortisone to Cortisol in Human Adipose Tissue 
Obesity (Silver Spring, Md.)  2008;16(6):1178-1185.
Our main objective was to compare the regulation of cortisol production within omental (Om) and abdominal subcutaneous (Abd sc) human adipose tissue.
Methods and Procedures
Om and Abd sc adipose tissue were obtained at surgery from subjects with a wide range of BMI. Hydroxysteroid dehydrogenase (HSD) activity (3H-cortisone and 3H-cortisol interconversion) and expression were measured before and after organ culture with insulin and/or dexamethasone.
Type 1 HSD (HSD1) mRNA and reductase activity were mainly expressed within adipocytes and tightly correlated with adipocyte size within both depots. There was no depot difference in HSD1 expression or reductase activity, while cortisol inactivation and HSD2 mRNA expression (expressed in stromal cells) were higher in Om suggesting higher cortisol turnover in this depot. Culture with insulin decreased HSD reductase activity in both depots. Culture with dexamethasone plus insulin compared to insulin alone increased HSD reductase activity only in the Om depot. This depot-specific increase in reductase activity could not be explained by an alteration in HSD1 mRNA or protein, which was paradoxically decreased. However, in Om only, hexose-6-phosphate dehydrogenase (H6PDH) mRNA levels were increased by culture with dexamethasone plus insulin compared to insulin alone, suggesting that higher nicotinamide adenine dinucleotide phosphate-oxidase (NADPH) production within the endoplasmic reticulum (ER) contributed to the higher HSD reductase activity.
We conclude that in the presence of insulin, glucocorticoids cause a depot-specific increase in the activation of cortisone within Om adipose tissue, and that this mechanism may contribute to adipocyte hypertrophy and visceral obesity.
PMCID: PMC4336796  PMID: 18388900
2.  Race modifies the association between adiposity and inflammation in patients with chronic kidney disease: findings from the CRIC study 
Obesity (Silver Spring, Md.)  2014;22(5):1359-1366.
To examine the race-specific association of inflammation with adiposity and muscle mass in subjects with chronic kidney disease (CKD).
Design and Methods
Plasma concentration of IL-1β, IL-Receptor antagonist (IL-1RA), IL-6, IL-10, TNF-α, TGF-β, hs-CRP, fibrinogen, and serum albumin were measured in 3,939 Chronic Renal Insufficiency Cohort study participants. Bioelectric impedance analysis was used to determine body fat mass (BFM) and fat free mass (FFM).
Plasma levels of hs-CRP, fibrinogen, IL-1RA, IL-6, and TNF-α increased and serum albumin decreased across the quartiles of body mass index. In multivariable analysis, BFM and FFM were positively associated with hs-CRP, fibrinogen, IL-1β, IL-1RA and IL-6. One standard deviation (SD) increase in BFM and FFM was associated with 0.36 (95% CI 0.33, 0.39) and 0.26 (95% CI 0.22, 0.30) SD increase in log transformed hs-CRP, respectively (p<0.001). Race stratified analysis showed that the association between biomarkers and BFM and FFM differed by race, with Caucasians demonstrating a stronger association with markers of inflammation than African Americans.
BFA and FFM are positively associated with markers of inflammation in patients with CKD. Race stratified analysis showed that Caucasians have a stronger association with markers of inflammation compared to African Americans.
PMCID: PMC4327849  PMID: 24415732
Bioelectric impedance analysis; cytokines; acute phase proteins; muscle mass; Body mass index; African Americans
3.  Shift-and-Persist: A Protective Factor for Elevated BMI Among Low-Socioeconomic-Status Children 
Obesity (Silver Spring, Md.)  2013;21(9):1759-1763.
Low socioeconomic status (SES) is associated with many adverse health outcomes, including childhood overweight and obesity. However, little is understood about why some children defy this trend by maintaining a healthy weight despite living in obesogenic environments. The objective of this study is to test the hypothesis that the psychological strategy of “shift-and-persist” protects low-SES children from overweight and obesity. Shift-and-persist involves dealing with stressors by reframing them more positively while at the same time persisting in optimistic thoughts about the future.
Design and Methods
Middle school children (N = 1,523, ages 9–15) enrolled in a school-based obesity prevention trial completed health surveys and physical assessments. Multiple linear regression analysis was used to examine the role of SES, shift-and-persist strategies, and their interaction on BMI z-scores, while controlling for student race/ethnicity, gender, and reported diet and physical activity.
Among children reporting engaging in less frequent shift-and-persist strategies, lower SES was associated with significantly higher BMI z-scores (P < 0.05). However, among children reporting engaging in more frequent shift-and-persist strategies, there was no association of SES with BMI z-score (P = 0.16), suggesting that shift-and-persist strategies may be protective against the association between SES and BMI.
Interventions aimed at improving psychological resilience among children of low SES may provide a complementary approach to prevent childhood overweight and obesity among at-risk populations.
PMCID: PMC4325991  PMID: 23671041
4.  A modified protocol to maximize differentiation of human preadipocytes and improve metabolic phenotypes 
Obesity (Silver Spring, Md.)  2012;20(12):2334-2340.
Adipose stromal cells proliferate and differentiate into adipocytes, providing a valuable model system for studies of adipocyte biology. We compared differentiation protocols for human preadipocytes and report on their metabolic phenotypes. By simply prolonging the adipogenic induction period from the first 3 days to 7 days, the proportion of cells (passage 5–6) acquiring adipocyte morphology increased from 30–70% to over 80% in human subcutaneous preadipocytes. These morphological changes were accompanied by increases in the adipogenic marker expression and improved adipocyte metabolic phenotypes: enhanced responses to beta-adrenergically-stimulated lipolysis and to insulin-stimulated glucose metabolism into triglyceride. Confirming previous studies, FBS dose-dependently inhibited adipogenesis. However, in subcutaneous preadipocytes that differentiate well (donor-dependant high capacity and subcultured fewer than 2 times), the use of 7d-induction protocols in both 3% FBS and serum-free conditions allowed >80% differentiation. Responsiveness to β-adrenergically stimulated lipolysis was lower in 3% FBS. Rates of insulin-stimulated glucose uptake were higher in adipocytes differentiated with 3% FBS, while the sensitivity to insulin was almost identical between the two groups. In summary, extending the length of the induction period in adipogenic cocktail improves the degree of differentiation and responses to key metabolic hormones. This protocol permits functional analysis of metabolic phenotypes in valuable primary human adipocyte cultures through multiple passages.
PMCID: PMC4320940  PMID: 22627913
5.  Obesity, Insulin Resistance, and Alzheimer’s Disease 
Obesity (Silver Spring, Md.)  2012;20(8):1549-1557.
PMCID: PMC4314950  PMID: 22310232
6.  Cognitive Performance and BMI in Childhood: Shared Genetic Influences Between Reaction Time But Not Response Inhibition 
Obesity (Silver Spring, Md.)  2014;22(11):2312-2318.
The aim of this work is to understand whether shared genetic influences can explain the association between obesity and cognitive performance, including slower and more variable reaction times (RTs) and worse response inhibition.
RT on a four-choice RT task and the go/no-go task, and commission errors on the go/no-go task for 1,312 twins ages 7-10 years were measured. BMI was measured at 9-12 years. Biometric twin models were run to give an estimate of the genetic correlation (rG) between body mass index (BMI) and three cognitive measures: mean RT (MRT), RT variability (RTV; the standard deviation of RTs), and commission errors (a measure of response inhibition).
Genetic correlations indicated that 20%-30% of the genes underlying BMI were shared with both RT measures. However, only small phenotypic correlations between MRT and RTV with later BMI (rPh = ~0.1) were observed. Commission errors were unassociated with later BMI (rPh = −0.03, ns).
Our results are the first to demonstrate significant shared genetic effects between RT performance and BMI. Our findings add biological support to the notion that obesity is associated with slower and more variable RTs. However, our results also emphasize the small nature of the association, which may explain previous negative findings.
PMCID: PMC4313367  PMID: 25376398
7.  [No title available] 
PMCID: PMC4005612  PMID: 23836764
8.  [No title available] 
PMCID: PMC4114995  PMID: 24777985
9.  [No title available] 
PMCID: PMC4115016  PMID: 24715468
10.  [No title available] 
PMCID: PMC4115026  PMID: 24634371
11.  [No title available] 
PMCID: PMC4115036  PMID: 24771588
12.  [No title available] 
PMCID: PMC4115048  PMID: 24852693
14.  CRF Type 2 Receptors Mediate the Metabolic Effects of Ghrelin in C2C12 cells 
Obesity (Silver Spring, Md.)  2013;22(2):380-389.
Ghrelin is known to regulate appetite control and cellular metabolism. The Corticotropin-Releasing Factor (CRF) family is also known to regulate energy balance. In this study, we investigated the links between ghrelin and the CRF family in C2C12 cells, a mouse myoblast cell line.
Design and methods
C2C12 cells were treated with ghrelin in the presence or absence of CRF receptor antagonists and then subjected to different metabolic analyses.
Ghrelin enhanced glucose uptake by C2C12 cells, induced GLUT4 translocation to the cell surface and decreased RBP4 expression. A CRF-R2 selective antagonist, anti-sauvagine-30, blocked ghrelin-induced glucose uptake, Ghrelin upregulated CRF-R2 but not CRF-R1 levels. Moreover, ghrelin-treated C2C12 cells displayed a cAMP and pERK activation in response to Ucn3, a CRF-R2 specific ligand, but not in response to CRF or stressin, CRF-R1 specific ligands. Ghrelin also induced UCP2 and UCP3 expression, which were blocked by anti-sauvagine-30. Ghrelin did not induce fatty acids uptake by C2C12 cells or ACC expression. Even though C2C12 cells clearly exhibited responses to ghrelin, the known ghrelin receptor, GHSR1a, was not detectable in C2C12 cells.
Our results suggest that, ghrelin plays a role in regulating muscle glucose and, raise the possibility that suppression of the CRF-R2 pathway might provide benefits in high ghrelin states.
PMCID: PMC4170921  PMID: 23804489
Ghrelin; CRF; metabolism; glocuse
15.  Identification of a novel lncRNA in gluteal adipose tissue and evidence for its positive effect on preadipocyte differentiation 
Obesity (Silver Spring, Md.)  2014;22(8):1781-1785.
Peripheral lower body fat is associated with lower cardiometabolic risk. Physiological differences in gluteal compared to abdominal subcutaneous (sc) adipocyte functions are known but the molecular basis for depot differences in adipocyte function is poorly understood.
To identify novel gene regulatory pathways that underlie the heterogeneity of human fat distribution.
Design and methods
Abdominal and gluteal adipose tissue aspirates obtained from 35 subjects (age=30±1.6 years; BMI=27.3±1.3kg/m2) were analyzed using Illumina microarrays and confirmed by RT-PCR. The HOTAIR gene was stably transfected into primary cultured human abdominal sc preadipocytes using a lentivirus and effects on adipogenic differentiation were analyzed.
We identified a long non-coding RNA, HOTAIR that was expressed in gluteal but not in Abd sc adipose tissue. This difference was retained throughout in vitro differentiation and was maximal at day 4. Ectopic expression of HOTAIR in abdominal preadipocytes produced an increase in differentiation as reflected by a higher percentage of differentiated cells, and increased expression of key adipogenic genes including PPARγ and LPL.
HOTAIR is expressed in gluteal adipose and may regulate key processes in adipocyte differentiation. The role of this lncRNA in determining the metabolic properties of gluteal compared to abdominal adipocytes merits further study.
PMCID: PMC4228784  PMID: 24862299
HOTAIR; Gluteal adipose tissue; adipogenic differentiation
16.  Racial Differences in Measures of Obesity and Risk of Colon Adenoma 
Obesity (Silver Spring, Md.)  2011;20(3):673-677.
Obesity is an established risk factor for several malignancies. However, the specific measurement of obesity most relevant to colon neoplasia is still debated, and evidence has suggested gender and racial differences in this measurement. In this study, we sought to compare which measurement—BMI, waist circumference (WC), waist-to-hip ratio (WHR) or waist-to-height ratio (WHtR)—is most strongly associated with development of colon adenomas, a precursor of colon cancer, and to investigate differences in this association between racial groups. We confirmed the strong association between WHR, as a measure of central obesity, and development of colon neoplasia. In our overall analysis, patients in the highest WHR quartile showed a substantial increase in risk of colon adenomas compared to patients in the lowest WHR quartile (odds ratio (OR) = 1.82, 95% confidence interval (CI): 1.12–2.71, Ptrend = 0.0017). In stratified analyses, we noted that strongly associated obesity measures in European Americans were WC (OR = 2.38, 95% CI = 1.45–3.92, Ptrend = 0.0004) and BMI (OR = 2.18, 95% CI = 1.37–3.49, Ptrend = 0.0015), whereas in African Americans, WHR was the strongest and the only obesity measure statistically significantly associated with adenoma risk (OR = 2.12, 95% CI = 1.05–4.30, Ptrend = 0.025). Our data highlight the importance of obesity in the development of early colon neoplasia and suggest substantial racial differences in the measures of obesity most strongly associated with risk of colon adenomas.
PMCID: PMC4301956  PMID: 21996657
17.  Resistance Training Preserves Fat-free Mass Without Impacting Changes in Protein Metabolism After Weight Loss in Older Women 
Obesity (Silver Spring, Md.)  2009;17(7):1332-1339.
This study assessed the effects of resistance training (RT) on energy restriction–induced changes in body composition, protein metabolism, and the fractional synthesis rate of mixed muscle proteins (FSRm) in postmenopausal, overweight women. Sixteen women (age 68 ± 1 years, BMI 29 ± 1 kg/m2, mean ± s.e.m.) completed a 16-week controlled diet study. Each woman consumed 1.0 g protein/kg/day. At baseline (weeks B1–B3) and poststudy (weeks RT12–RT13), energy intake matched each subject’s need and during weeks RT1–RT11 was hypoenergetic by 2,092 kJ/day (500 kcal/day). From weeks RT1 to RT13, eight women performed RT 3 day/week (RT group) and eight women remained sedentary (SED group). RT did not influence the energy restriction–induced decrease in body mass (SED −5.8 ± 0.6 kg; RT −5.0 ± 0.2 kg) and fat mass (SED −4.1 ± 0.9 kg; RT −4.7 ± 0.5 kg). Fat-free mass (FFM) and total body water decreased in SED (−1.6 ± 0.4 and −2.1 ± 0.5 kg) and were unchanged in RT (−0.3 ± 0.4 and −0.4 ± 0.7 kg) (group-by-time, P ≤ 0.05 and P = 0.07, respectively). Protein–mineral mass did not change in either group (SED 0.4 ± 0.2 kg; RT 0.1 ± 0.4 kg). Nitrogen balance, positive at baseline (2.2 ± 0.3 g N/day), was unchanged poststudy. After body mass loss, postabsorptive (PA) and postprandial (PP) leucine turnover, synthesis, and breakdown decreased. Leucine oxidation and balance were not changed. PA and total (PA + PP) FSRm in the vastus lateralis were higher after weight loss. RT did not influence these protein metabolism responses. In summary, RT helps older women preserve FFM during body mass loss. The comparable whole-body nitrogen retentions, leucine kinetics, and FSRm between groups are consistent with the lack of differential protein–mineral mass change.
PMCID: PMC4299870  PMID: 19247271
18.  Food form and portion size affect postprandial appetite sensations and hormonal responses in healthy, non-obese, older adults 
Obesity (Silver Spring, Md.)  2009;18(2):293-299.
Data are limited concerning the dietary factors that influence appetite control in older adults. This study examined the effects of food form (FF) and portion size (PS) on appetite in 43 older adults (age: 72±1 y; BMI: 25.6±0.3 kg/m2). Subjects were assigned to groups based on PS of the test-meal (12.5% (n=18) vs. 25% (n=25) of estimated energy need). Subjects randomly consumed, on 2 separate days, the respective solid (S) or beverage (B) test-meal. Appetite sensations and hormonal responses were measured over 4 h. Main effects of FF (p<0.05) and/or PS (p<0.05) were observed for each appetite sensation. Postprandial hunger and desire to eat were greater following B vs. S and between 12.5% vs. 25%, whereas fullness was lower after B vs. S (p<0.05). Main effects of FF and/or PS were observed for glucose, insulin, and ghrelin. Postprandial glucose and insulin concentrations were lower after B vs. S and between 12.5% vs. 25% (all comparisons, p<0.05) while B led to greater 4-h ghrelin vs. S (p=0.09). No main effects were observed for GLP-1 or CCK. When adjusting for age, FF remained significant for postprandial hunger and fullness; PS remained significant for postprandial glucose. Greater hunger and reduced satiety with accompanying glucose, insulin, and ghrelin following the beverage vs. solid meals, and to some extent, in smaller vs. larger portions suggest that appetite control is influenced by food form and portion size in older adults. These findings may enhance the development of appropriate dietary strategies to help regulate energy balance.
PMCID: PMC4297632  PMID: 19629055
food rheology; portion sizes; elderly; appetite; beverages; ghrelin
19.  Metabolic Syndrome is linked to Chromosome 7q21 and associated with genetic variants in CD36 and GNAT3 in Mexican Americans 
Obesity (Silver Spring, Md.)  2012;20(10):2083-2092.
The prevalence of metabolic syndrome (MS) has been rising alarmingly worldwide, including in the United States, but knowledge on specific genetic determinants of MS is very limited. Therefore, we planned to identify the genetic determinants of MS as defined by National Cholesterol Education Program/Adult Treatment Panel III (NCEP/ATPIII) criteria. We performed linkage screen for MS using data from 692 Mexican Americans, who participated in the San Antonio Family Diabetes/Gallbladder Study (SAFDGS). We found strong evidence for linkage of MS on chromosome 7q (LOD = 3.6, empirical P = 6.0 × 10−5), between markers D7S2212 and D7S821. In addition, six chromosomal regions exhibited potential evidence for linkage (LOD ≥ 1.2) with MS. Further, we examined 29 single nucleotide polymorphisms (SNPs) from the fatty acid translocase (FAT or CD36, 18 SNPs) gene and guanine nucleotide binding protein, alpha transducing 3 (GNAT3, 11 SNPs) gene, located within the 1-LOD support interval region for their association with MS and its related traits. Several SNPs were associated with MS and its related traits. Remarkably, rs11760281 in GNAT3 and rs1194197 near CD36 exhibited the strongest associations with MS (P = 0.0003, relative risk [RR] = 1.6 and P = 0.004, RR = 1.7 respectively) and several other related traits. These two variants explained about 18% of the MS linkage evidence on chromosome 7q21, and together conferred approximately 3-fold increase in MS risk (RR = 2.7). In conclusion, our linkage and subsequent association studies implicate a region on chromosome 7q21 to influence MS in Mexican Americans.
PMCID: PMC4287372  PMID: 22456541
Metabolic syndrome; NCEP/ATPIII; linkage/genome scan; variance components linkage analysis; single nucleotide polymorphisms; association analysis; Mexican Americans; CD36/FAT; GNAT3
20.  Canagliflozin: Effects in overweight and obese subjects without diabetes mellitus 
Obesity (Silver Spring, Md.)  2013;22(4):1042-1049.
To evaluate the effects of canagliflozin, a sodium glucose co-transporter 2 inhibitor, on body weight in overweight and obese subjects (body mass index [BMI] ≥27 and <50 kg/m2).
This 12-week, Phase 2b, randomized, double-blind study enrolled 376 subjects without diabetes mellitus who received canagliflozin 50, 100, or 300 mg or placebo once daily. The primary endpoint was the percent change in body weight from baseline through Week 12.
Canagliflozin increased urinary glucose excretion in a dose-dependent manner and produced statistically significant reductions in body weight compared with placebo (least squares mean percent changes from baseline of −2.2%, −2.9%, −2.7%, and −1.3% with canagliflozin 50, 100, and 300 mg and placebo; P < 0.05 for all comparisons). Overall adverse event (AE) rates were similar across groups. Canagliflozin was associated with higher rates of genital mycotic infections in women, which were generally mild and led to few study discontinuations. Osmotic diuresis-related AE rates were low and similar across groups.
In overweight and obese subjects without diabetes mellitus, canagliflozin significantly reduced body weight compared with placebo and was generally well tolerated.
PMCID: PMC4285787  PMID: 24227660
21.  Associations Between Obesity and Changes in Adult BMI Over Time and Colon Cancer Risk 
Obesity (Silver Spring, Md.)  2008;16(5):1099-1104.
Obesity has been associated with increased colon cancer risk in epidemiological studies; however, the specific time periods during which obesity may be most relevant as well as how changes in adult body size over time affect colon cancer risk have not been well explored. We evaluated potential associations between BMI in each age decade (20s, 30s, 40s, 50s, and 2 years before study recruitment (“recruitment period”)) and in BMI changes over time and colon cancer risk in a population-based case–control study comprising 438 cases and 491 controls. We found that obese (BMI ≥ 30.0 kg/m2) compared to normal (BMI ≥ 18.5 to <25.0 kg/m2) body size at the recruitment period was associated with increased colon cancer risk (odds ratio (OR) = 1.54; 95% confidence interval (CI) = 1.03–2.31; P = 0.03). No associations were observed for obese body size in the other age decades. An increased risk was found for changes in BMI between the 30s decade and the recruitment period of 5–10 kg/m2 (OR = 1.54; 95% CI = 1.02–2.34; P = 0.04) and >10 kg/m2 (OR = 2.40; 95% CI = 1.23–4.66; P = 0.01) (P trend = 0.01). Stratification by gender revealed that BMI changes >10 kg/m2 increased risk in women but not men. Similar results were found for BMI changes between the 20s decade and the recruitment period but effect sizes were smaller. Our results provide additional support for obesit's role in colon cancer and suggest large body size increases exceeding 10 kg/m2 may potentially be more important after age 30, particularly among women; however, prospective studies with sex hormone, growth factor, and pro-inflammatory biomarkers are needed to provide insights to the underlying biological mechanism(s).
PMCID: PMC4284816  PMID: 18356841
22.  Deletion of TNF-Like Weak Inducer of Apoptosis (TWEAK) Protects Mice From Adipose and Systemic Impacts of Severe Obesity 
Obesity (Silver Spring, Md.)  2014;22(6):1485-1494.
To investigate the role of TNF-like weak inducer of apoptosis (TWEAK) in pathological adipose tissue (AT) remodeling and complications of obesity.
Design and Methods
Wild type (WT) and TWEAK knockout (KO) mice were fed normal diet (ND) or a high fat diet (HFD) for up to 17 weeks. Adipocyte death was induced using an established transgenic mouse model of inducible adipocyte apoptosis (FAT-ATTAC). Metabolic, biochemical, histologic and flow cytometric analyses were performed.
TWEAK and its receptor, fibroblast growth factor-inducible molecule 14 (Fn14) were upregulated in gonadal (g)AT of WT mice after HFD week 4 and 24 h after induction of adipocyte apoptosis. Phenotypes of KO and WT mouse were indistinguishable through HFD week 8. However, at week 17 obese KO mice had ~30% larger gAT adipocytes and gAT mass than WT mice, coincident with reduced adipocyte death, enhanced insulin signaling, Th2/M2 immune skewing, fewer thick collagen fibers, and altered expression of extracellular matrix constituents and modulators that is consistent with reduced fibrosis and larger adipocytes. KO mice were less steatotic and became more insulin sensitive and glucose tolerant than WT mice after HFD week 12.
TWEAK constrains ‘healthy’ gAT expansion and promotes metabolic complications in severe obesity.
PMCID: PMC4283503  PMID: 24616441
TWEAK; adipose tissue; obesity; fibrosis; inflammation; insulin resistance
23.  Pass the Popcorn: “Obesogenic” Behaviors and Stigma in Children’s Movies 
Obesity (Silver Spring, Md.)  2013;22(7):1694-1700.
To determine the prevalence of obesity-related behaviors and attitudes in children’s movies.
Design and Methods
We performed a mixed-methods study of the top-grossing G- and PG-rated movies, 2006–2010 (4 per year). For each 10-minute movie segment the following were assessed: 1) prevalence of key nutrition and physical activity behaviors corresponding to the American Academy of Pediatrics obesity prevention recommendations for families; 2) prevalence of weight stigma; 3) assessment as healthy, unhealthy, or neutral; 3) free-text interpretations of stigma.
Agreement between coders was greater than 85% (Cohen’s kappa=0.7), good for binary responses. Segments with food depicted: exaggerated portion size (26%); unhealthy snacks (51%); sugar-sweetened beverages (19%). Screen time was also prevalent (40% of movies showed television; 35% computer; 20% video games). Unhealthy segments outnumbered healthy segments 2:1. Most (70%) of the movies included weight-related stigmatizing content (e.g. “That fat butt! Flabby arms! And this ridiculous belly!”).
These popular children’s movies had significant “obesogenic” content, and most contained weight-based stigma. They present a mixed message to children: promoting unhealthy behaviors while stigmatizing the behaviors’ possible effects. Further research is needed to determine the effects of such messages on children.
PMCID: PMC4004726  PMID: 24311390
Childhood obesity; children; stigma; weight-related teasing; movies
24.  An 8-Month Randomized Controlled Exercise Trial Alters Brain Activation During Cognitive Tasks in Overweight Children 
Obesity (Silver Spring, Md.)  2013;22(1):232-242.
Children who are less fit reportedly have lower performance on tests of cognitive control and differences in brain function. This study examined the effect of an exercise intervention on brain function during two cognitive control tasks in overweight children.
Design and Methods
Participants included 43 unfit, overweight (BMI ≥ 85th percentile) children 8- to 11-years old (91% Black), who were randomly divided into either an aerobic exercise (n = 24) or attention control group (n = 19). Each group was offered a separate instructor-led after-school program every school day for 8 months. Before and after the program, all children performed two cognitive control tasks during functional magnetic resonance imaging (fMRI): antisaccade and flanker.
Compared to the control group, the exercise group decreased activation in several regions supporting antisaccade performance, including precentral gyrus and posterior parietal cortex, and increased activation in several regions supporting flanker performance, including anterior cingulate and superior frontal gyrus.
Exercise may differentially impact these two task conditions, or the paradigms in which cognitive control tasks were presented may be sensitive to distinct types of brain activation that show different effects of exercise. In sum, exercise appears to alter efficiency or flexible modulation of neural circuitry supporting cognitive control in overweight children.
PMCID: PMC4077546  PMID: 23788510
25.  Spexin is a Novel Human Peptide that Reduces Adipocyte Uptake of Long Chain Fatty Acids and Causes Weight Loss in Rodents with Diet-induced Obesity* 
Obesity (Silver Spring, Md.)  2014;22(7):1643-1652.
Microarray studies identified Ch12:orf39 (Spexin) as the most dysregulated gene in obese human fat. Therefore we examined its role in obesity pathogenesis.
Design and Methods
Spexin effects on food intake, meal patterns, body weight, Respiratory Exchange Ratio (RER), and locomotor activity were monitored electronically in C57BL/6J mice or Wistar rats with dietary-induced obesity (DIO). Its effects on adipocyte [3H]-oleate uptake were determined.
In humans, Spexin gene expression was down-regulated 14.9-fold in obese omental and subcutaneous fat. Circulating Spexin changed in parallel, correlating (r = −0.797) with Leptin. In rats, Spexin (35 μg/kg/day s.c) reduced caloric intake ~32% with corresponding weight loss. Meal patterns were unaffected. In mice, Spexin (25 μg/kg/day i.p.) significantly reduced the RER at night, and increased locomotion. Spexin incubation in vitro significantly inhibited facilitated fatty acid (FA) uptake into DIO mouse adipocytes. Conditioned taste aversion testing (70μg/kg/day i.p.) demonstrated no aversive Spexin effects.
Spexin gene expression is markedly down-regulated in obese human fat. The peptide produces weight loss in DIO rodents. Its effects on appetite and energy regulation are presumably central; those on adipocyte FA uptake appear direct and peripheral. Spexin is a novel hormone involved in weight regulation, with potential for obesity therapy.
PMCID: PMC4077920  PMID: 24550067

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