Perceived Stress and Weight Gain in Adolescence: A Longitudinal Analysis

Perceived Stress and Weight Gain in Adolescence: A Longitudinal Analysis

Cornelia H.M. van Jaarsveld1, Jennifer A. Fidler1, Andrew Steptoe2, David Boniface1 and Jane Wardle1
1Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London, UK
2Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, UK

Abstract

Although perceived stress has been hypothesized to be a risk factor for obesity, epidemiological studies relating stress to weight gain have shown mixed results. We examined prospective associations between perceived stress and changes in waist circumference and BMI in a large study of adolescents. As part of the Health and Behaviour in Teenagers Study (HABITS), height, weight, and waist circumference were measured annually in 4,065 adolescents aged from 11 to 16. Waist and BMI standard deviation scores (SDS) were used as indices of adiposity. Adolescents completed a measure of perceived stress each year, from which mean stress scores over the 5-year period were also calculated and divided by tertile into lower, moderate, and higher stress. Associations between perceived stress at each year and adiposity 1–4 years later and also adiposity trajectories over the whole period in relation to mean stress were investigated. Analyses were adjusted for age, sex, ethnicity, socioeconomic deprivation, pubertal timing, and smoking. Perceived stress in any year was not related prospectively to increases in waist or BMI SDS 1–4 years later, nor was there any evidence that higher stress over the whole period was associated with greater gains in waist or BMI SDS. However, waist and BMI SDS were significantly higher in the moderate- and higher-stress groups than the lower-stress group across the whole 5-year period. Persistent stress was associated with higher waist circumference and BMI in adolescence, but did not lead to differential changes over 5 years.

Antiobesity Effects of yerba maté Extract (Ilex paraguariensis) in High-fat Diet–induced Obese Mice

Antiobesity Effects of yerba maté Extract (Ilex paraguariensis) in High-fat Diet–induced Obese Mice

Demétrius P. Arçari1,2, Waldemar Bartchewsky1, Tanila W. dos Santos1, Karim A. Oliveira1, Alexandre Funck1, José Pedrazzoli1, Marina F.F. de Souza2, Mario J. Saad3, Deborah H.M. Bastos2, Alessandra Gambero1, Patricia de O. Carvalho4 and Marcelo L. Ribeiro1
1Unidade Integrada de Farmacologia e Gastroenterologia, Universidade São Francisco, Bragança Paulista, Brazil
2Departamento de Nutrição, Faculdade de Saúde Publica, Universidade de São Paulo, São Paulo, Brazil
3Departamento de Medicina Interna UNICAMP, Campinas, Brazil
4Laboratório Multidisciplinar de Pesquisa, Universidade São Francisco, Bragança Paulista, Brazil

Abstract

Because the potential of yerba maté (Ilex paraguariensis) has been suggested in the management of obesity, the aim of the present study was to evaluate the effects of yerba maté extract on weight loss, obesity-related biochemical parameters, and the regulation of adipose tissue gene expression in high-fat diet–induced obesity in mice. Thirty animals were randomly assigned to three groups. The mice were introduced to standard or high-fat diets. After 12 weeks on a high-fat diet, mice were randomly assigned according to the treatment (water or yerba maté extract 1.0 g/kg). After treatment intervention, plasma concentrations of total cholesterol, high-density lipoprotein cholesterol, triglyceride, low-density lipoprotein (LDL) cholesterol, and glucose were evaluated. Adipose tissue was examined to determine the mRNA levels of several genes such as tumor necrosis factor- (TNF-), leptin, interleukin-6 (IL-6), C-C motif chemokine ligand-2 (CCL2), CCL receptor-2 (CCR2), angiotensinogen, plasminogen activator inhibitor-1 (PAI-1), adiponectin, resistin, peroxisome proliferator-activated receptor-2 (PPAR-2), uncoupling protein-1 (UCP1), and PPAR- coactivator-1 (PGC-1). The F4/80 levels were determined by immunoblotting. We found that obese mice treated with yerba maté exhibited marked attenuation of weight gain, adiposity, a decrease in epididymal fat-pad weight, and restoration of the serum levels of cholesterol, triglycerides, LDL cholesterol, and glucose. The gene and protein expression levels were directly regulated by the high-fat diet. After treatment with yerba maté extract, we observed a recovery of the expression levels. In conclusion, our data show that yerba maté extract has potent antiobesity activity in vivo. Additionally, we observed that the treatment had a modulatory effect on the expression of several genes related to obesity.

A Meta-Analysis Evaluating the Impact of Chitosan on Serum Lipids in Hypercholesterolemic Patients

A Meta-Analysis Evaluating the Impact of Chitosan on Serum Lipids in Hypercholesterolemic Patients

William L. Bakera, c, Alix Terciusb, Moise Angladeb, C. Michael Whitea, c, Craig I. Colemana, c

University of Connecticut Schools of
aPharmacy and
bMedicine, Storrs, Conn. and Farmington, Conn., and
cEvidence-Based Practice Center at Hartford Hospital, Hartford, Conn., USA

Address of Corresponding Author

Ann Nutr Metab 2009;55:368-374 (DOI: 10.1159/000258633)

Key Words
Chitin
Chitosan
Hypercholesterolemia
Meta-analysis

Abstract

Background/Objective: Chitosan is increasingly being used in the United States as an over-the-counter cholesterol-lowering agent. The positively charged amino groups of chitosan may have the ability to bind negatively charged molecules such as lipids and bile acids, inducing a greater fractional excretion in the feces. To better characterize the impact of chitosan on serum lipids in hypercholesterolemic patients, we performed a meta-analysis of randomized controlled trials. Methods: A systematic literature search of Medline, Embase, Cochrane Central and the Natural Medicines Comprehensive Database was conducted from the earliest possible date through May 2008. Trials were included in the analysis if they were randomized, placebo-controlled trials of chitosan in hypercholesterolemic patients and reported efficacy data on total, low-density lipoprotein (LDL), high-density lipoprotein (HDL) cholesterol or triglycerides. The weighted mean difference (WMD) of the change from baseline (in milligrams per deciliter) with 95% confidence interval was calculated as the difference between the mean in the chitosan and placebo groups using a random-effects model. Results: Six studies (n = 416 patients) met the inclusion criteria. Upon meta-analysis, the use of chitosan significantly lowered total cholesterol [WMD, -11.59 mg/dl (-21.45 to -1.73), p = 0.02] but not LDL cholesterol, HDL cholesterol or triglycerides.

Conclusions: Based upon the currently available literature, we can only say that chitosan beneficially affects total cholesterol with 95% confidence. Additional, larger randomized controlled trials are needed to better characterize the effect of chitosan on other lipoproteins.

Sustained participation in youth sport decreases metabolic syndrome in adulthood

Sustained participation in youth sport decreases metabolic syndrome in adulthood

X Yang1, R Telama2, M Hirvensalo2, J S A Viikari3 and O T Raitakari4
1LIKES Research Center for Sport and Health Sciences, Jyväskylä, Finland
2Department of Sport Sciences, University of Jyväskylä, Jyväskylä, Finland
3Department of Medicine, University of Turku, Turku, Finland
4Department of Clinical Physiology, University of Turku, Turku, Finland

Correspondence: Dr X Yang, LIKES Research Center for Sport and Health Sciences, Yliopistonkatu 20, Jyväskylä 40100, Finland. E-mail: xiaolin.yang@likes.fi

Received 13 May 2009; Revised 18 June 2009; Accepted 28 June 2009; Published online 1 September 2009.

Abstract
Objective: to explore the effect of organized youth sport on metabolic syndrome (MetS) in adulthood.
Design: Longitudinal study data from the cardiovascular risk in young Finns study.
Subjects: A total of 1493 males (n=704) and females (n=789) aged 3, 6, 9, 12, 15 and 18 years were randomly selected from five university towns and their rural surroundings in 1980. They were followed up for 21 years. In 2001 they were 24, 27, 30, 33, 36 and 39 years old.
Measurements: Youth sports participation data (participation in sport-club training and competitions) were assessed in 1980 and 1983 using a self-report questionnaire completed in connection with a medical examination. Participants were divided into athletes and non-athletes at each measurement point, and then classified into four groups: Persistent athlete, Starter, Leaver and Non-athlete. A mean score of youth sport was assessed by calculating the average of four consecutive measurements (1980–1989). MetS risk in 2001 was defined as a categorical variable based on the guidelines of the European Group for the Study of Insulin Resistance (EGIR) and as a continuous MetS-score variable by summing the z-scores of individual metabolic variables.
Results: In males and females, intense participation in youth sports over 3 years was inversely and significantly associated with clustered MetS score and prevalence of MetS defined by EGIR in adulthood (P<0.05). The association remained significant after adjustment for age, baseline clustered MetS score, smoking and total caloric intake and after additional adjustments for adult leisure-time physical activity. Starters during 3 years were less likely to have MetS than non-athletes. Leavers were at a higher risk for MetS than persistent athletes. These associations were attenuated in males by adjustment for all potential confounders. Similar associations were found using EGIR MetS as an outcome.
Conclusions: Sustained participation in organized sport lasting at least 3 years in youth is associated with reduced risk for developing MetS in adulthood.

Alcohol as a Risk Factor for Type 2 Diabetes: A systematic review and meta-analysis

Alcohol as a Risk Factor for Type 2 Diabetes: A systematic review and meta-analysis

by Baliunas, D. O., Taylor, B. J., Irving, H., Roerecke, M., Patra, J., Mohapatra, S., Rehm, J.

OBJECTIVE 

To clarify the dose-response relationship between alcohol consumption and type 2 diabetes.

RESEARCH DESIGN AND METHODS 

A systematic computer-assisted and hand search was conducted to identify relevant articles with longitudinal design and quantitative measurement of alcohol consumption. Adjustment was made for the sick-quitter effect. We used fractional polynomials in a meta-regression to determine the dose-response relationships by sex and end point using lifetime abstainers as the reference group.

RESULTS 

The search revealed 20 cohort studies that met our inclusion criteria. A U-shaped relationship was found for both sexes. Compared with lifetime abstainers, the relative risk (RR) for type 2 diabetes among men was most protective when consuming 22 g/day alcohol (RR 0.87 [95% CI 0.76–1.00]) and became deleterious at just over 60 g/day alcohol (1.01 [0.71–1.44]). Among women, consumption of 24 g/day alcohol was most protective (0.60 [0.52–0.69]) and became deleterious at about 50 g/day alcohol (1.02 [0.83–1.26]).

CONCLUSIONS 

Our analysis confirms previous research findings that moderate alcohol consumption is protective for type 2 diabetes in men and women.

Sleep Duration, Lifestyle Intervention, and Incidence of Type 2 Diabetes in Impaired Glucose Tolerance: The Finnish Diabetes Prevention Study

Sleep Duration, Lifestyle Intervention, and Incidence of Type 2 Diabetes in Impaired Glucose Tolerance: The Finnish Diabetes Prevention Study

by Tuomilehto, H., Peltonen, M., Partinen, M., Lavigne, G., Eriksson, J. G., Herder, C., Aunola, S., Keinanen-Kiukaanniemi, S., Ilanne-Parikka, P., Uusitupa, M., Tuomilehto, J., Lindstrom, J., on behalf of the Finnish Diabetes Prevention Study Group

OBJECTIVE 

Both short and long sleep duration have frequently been found to be associated with an increased risk for diabetes. The aim of the present exploratory analysis was to examine the association between sleep duration and type 2 diabetes after lifestyle intervention in overweight individuals with impaired glucose tolerance in a 7-year prospective follow-up.

RESEARCH DESIGN AND METHODS 

A total of 522 individuals (aged 40–64 years) were randomly allocated either to an intensive diet-exercise counseling group or to a control group. Diabetes incidence during follow-up was calculated according to sleep duration at baseline. Sleep duration was obtained for a 24-h period. Physical activity, dietary intakes, body weight, and immune mediators (C-reactive protein and interleukin-6) were measured.

RESULTS 

Interaction between sleep duration and treatment group was statistically significant (P = 0.003). In the control group, the adjusted hazard ratios (HRs) (95% CI) for diabetes were 2.29 (1.38–3.80) and 2.74 (1.67–4.50) in the sleep duration groups 9–9.5 h and ?10 h, respectively, compared with for that of the 7–8.5 h group. In contrast, sleep duration did not influence the incidence of diabetes in the intervention group; for sleep duration groups 9–9.5 h and ?10 h, the adjusted HRs (95% CI) were 1.10 (0.60–2.01) and 0.73 (0.34–1.56), respectively, compared with that in the reference group (7–8.5 h sleep). Lifestyle intervention resulted in similar improvement in body weight, insulin sensitivity, and immune mediator levels regardless of sleep duration.

CONCLUSIONS 

Long sleep duration is associated with increased type 2 diabetes risk. Lifestyle intervention with the aim of weight reduction, healthy diet, and increased physical activity may ameliorate some of this excess risk.

Eat less and exercise more - is it really enough to knock down the obesity pandemia?

Eat less and exercise more - is it really enough to knock down the obesity pandemia?

Hubácek JA.

Institute for Clinical and Experimental Medicine-CEM-LMG, Prague, Czech Republic. jahb@ikem.cz.

Reduced physical activity and abundant energy intake are two most common factors leading to uncontrolled body weight gain. But these factors are not under entire internal consciousness control; they are also partially genetically determined and are affected by for example food marketing practices. In addition to these two widely accepted factors, there are some other factors, whose could also contribute to the recent increase of obesity prevalence. For example, non-exercise activity thermogenesis, sleeping habits, more stable inside room temperatures (using of heating and air conditioning), high prescription of medications with weight gain as side effect, psychosocial factors, unfavourable socioeconomic status and unpleasant urban environment are the background factors which should not be omitted if obesity/BMI determination should be fully understood and kept under control. In conclusion, unhealthy life style is necessary, but not sufficient for obesity development.

Viral obesity: fact or fiction?

Viral obesity: fact or fiction?

Mitra AK, Clarke K.

Department of Community Health Sciences, The University of Southern Mississippi, Hattiesburg, MS, USA.

Summary The aetiology of obesity is multifactorial. An understanding of the contributions of various causal factors is essential for the proper management of obesity. Although it is primarily thought of as a condition brought on by lifestyle choices, recent evidence shows there is a link between obesity and viral infections. Numerous animal models have documented an increased body weight and a number of physiologic changes, including increased insulin sensitivity, increased glucose uptake and decreased leptin secretion that contribute to an increase in body fat in adenovirus-36 infection. Other viral agents associated with increasing obesity in animals included canine distemper virus, rous-associated virus 7, scrapie, Borna disease virus, SMAM-1 and other adenoviruses. This review attempted to determine if viral infection is a possible cause of obesity. Also, this paper discussed mechanisms by which viruses might produce obesity. Based on the evidence presented in this paper, it can be concluded that a link between obesity and viral infections cannot be ruled out. Further epidemiologic studies are needed to establish a causal link between the two, and determine if these results can be used in future management and prevention of obesity.

Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY and Glucagon-Like Peptide-1.

Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY and Glucagon-Like Peptide-1.

Kokkinos A, le Roux CW, Alexiadou K, Tentolouris N, Vincent RP, Kyriaki D, Perrea D, Ghatei MA, Bloom SR, Katsilambros N.

First Department of Propaedeutic Medicine (A.K., K.A., N.T., D.K., D.P., N.K.), Athens University Medical School, Laiko General Hospital, 11527 Athens, Greece; and Department of Metabolic Medicine (C.W.l.R., R.P.V., M.A.G., S.R.B.), Hammersmith Hospital, Imperial College, London W12 ONN, United Kingdom.

Context: The rate at which people eat has been suggested to be positively associated with obesity, although appetite and related gut hormones have not been measured. Objective: The objective of the study was to determine whether eating the same meal at varying speeds elicits different postprandial gut peptide responses. Design and Setting: This was a crossover study at a clinical research facility. Study Participants: Seventeen healthy adult male volunteers participated in the study. Intervention: A test meal consisting of 300 ml ice cream (675 kcal) was consumed in random order on two different sessions by each subject: meal duration took either 5 or 30 min. Main Outcome Measures: The postprandial response of the orexigenic hormone ghrelin and the anorexigenic peptides peptide YY and glucagon-like peptide-1 over 210 min was assessed. Visual analog scales for the subjective feelings of hunger and fullness were completed throughout each session. Results: Peptide YY area under the curve (AUC) was higher after the 30-min meal than after the 5-min meal (mean +/- SEM AUC 5 min meal: 4133 +/- 324, AUC 30 min meal: 5250 +/- 330 pmol/liter . min, P = 0.004), as was glucagon-like peptide-1 AUC (mean +/- SEM AUC 5 min meal: 6219 +/- 256, AUC 30 min meal: 8794 +/- 656 pmol/liter . min, P = 0.001). There was a trend for higher visual analog scale fullness ratings immediately after the end of the 30-min meal compared with immediately after the 5-min meal. There were no differences in ghrelin response. Conclusions: Eating at a physiologically moderate pace leads to a more pronounced anorexigenic gut peptide response than eating very fast.

The energy expenditure of using a "walk-and-work" desk for office workers with obesity.

The energy expenditure of using a "walk-and-work" desk for office workers with obesity.

Levine JA, Miller JM.

Endocrine Research Unit, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA. levine.james@mayo.edu

OBJECTIVE: For many people, most of the working day is spent sitting in front of a computer screen. Approaches for obesity treatment and prevention are being sought to increase workplace physical activity because low levels of physical activity are associated with obesity. Our hypothesis was that a vertical workstation that allows an obese individual to work while walking would be associated with significant and substantial increases in energy expenditure over seated work. METHODS: The vertical workstation is a workstation that allows an office worker to use a standard personal computer while walking on a treadmill at a self-selected velocity. 15 sedentary individuals with obesity (14 women, one man; 43 (7.5) years, 86 (9.6) kg; body mass index 32 (2.6) kg/m(2)) underwent measurements of energy expenditure at rest, seated working in an office chair, standing and while walking at a self-selected speed using the vertical workstation. Body composition was measured using dual x ray absorptiometry. RESULTS: The mean (SD) energy expenditure while seated at work in an office chair was 72 (10) kcal/h, whereas the energy expenditure while walking and working at a self-selected velocity of 1.1 (0.4) mph was 191 (29) kcal/h. The mean (SD) increase in energy expenditure for walking-and-working over sitting was 119 (25) kcal/h. CONCLUSIONS: If sitting computer-time were replaced by walking-and-working, energy expenditure could increase by 100 kcal/h. Thus, if obese individuals were to replace time spent sitting at the computer with walking computer time by 2-3 h/day, and if other components of energy balance were constant, a weight loss of 20-30 kg/year could occur.

Effect of cocoa powder on the modulation of inflammatory biomarkers in patients at high risk of cardiovascular disease

Effect of cocoa powder on the modulation of inflammatory biomarkers in patients at high risk of cardiovascular disease 

[Cardiovascular disease risk]

from American Journal of Clinical Nutrition current issue by Monagas, M., Khan, N., Andres-Lacueva, C., Casas, R., Urpi-Sarda, M., Llorach, R., Lamuela-Raventos, R. M., Estruch, R.

Background: Epidemiologic studies have suggested that flavonoid intake plays a critical role in the prevention of coronary heart disease. Because atherosclerosis is considered a low-grade inflammatory disease, some feeding trials have analyzed the effects of cocoa (an important source of flavonoids) on inflammatory biomarkers, but the results have been controversial.

Objective: The objective was to evaluate the effects of chronic cocoa consumption on cellular and serum biomarkers related to atherosclerosis in high-risk patients.

Design: Forty-two high-risk volunteers (19 men and 23 women; mean ± SD age: 69.7 ± 11.5 y) were included in a randomized crossover feeding trial. All subjects received 40 g cocoa powder with 500 mL skim milk/d (C+M) or only 500 mL skim milk/d (M) for 4 wk. Before and after each intervention period, cellular and serum inflammatory biomarkers related to atherosclerosis were evaluated.

Results: Adherence to the dietary protocol was excellent. No significant changes in the expression of adhesion molecules on T lymphocyte surfaces were found between the C+M and M groups. However, in monocytes, the expression of VLA-4, CD40, and CD36 was significantly lower (P = 0.005, 0.028, and 0.001, respectively) after C+M intake than after M intake. In addition, serum concentrations of the soluble endothelium-derived adhesion molecules P-selectin and intercellular adhesion molecule-1 were significantly lower (both P = 0.007) after C+M intake than after M intake.

Conclusions: These results suggest that the intake of cocoa polyphenols may modulate inflammatory mediators in patients at high risk of cardiovascular disease. These antiinflammatory effects may contribute to the overall benefits of cocoa consumption against atherosclerosis.

Short-term modified alternate-day fasting: a novel dietary strategy for weight loss and cardioprotection in obese adults

Short-term modified alternate-day fasting: a novel dietary strategy for weight loss and cardioprotection in obese adults 

[Obesity and eating disorders]

from American Journal of Clinical Nutrition current issue by Varady, K. A, Bhutani, S., Church, E. C, Klempel, M. C

Background: The ability of modified alternate-day fasting (ADF; ie, consuming 25% of energy needs on the fast day and ad libitum food intake on the following day) to facilitate weight loss and lower vascular disease risk in obese individuals remains unknown.

Objective: This study examined the effects of ADF that is administered under controlled compared with self-implemented conditions on body weight and coronary artery disease (CAD) risk indicators in obese adults.

Design: Sixteen obese subjects (12 women, 4 men) completed a 10-wk trial, which consisted of 3 phases: 1) a 2-wk control phase, 2) a 4-wk weight loss/ADF controlled food intake phase, and 3) a 4-wk weight loss/ADF self-selected food intake phase.

Results: Dietary adherence remained high throughout the controlled food intake phase (days adherent: 86%) and the self-selected food intake phase (days adherent: 89%). The rate of weight loss remained constant during controlled food intake (0.67 ± 0.1 kg/wk) and self-selected food intake phases (0.68 ± 0.1 kg/wk). Body weight decreased (P < 0.001) by 5.6 ± 1.0 kg (5.8 ± 1.1%) after 8 wk of diet. Percentage body fat decreased (P < 0.01) from 45 ± 2% to 42 ± 2%. Total cholesterol, LDL cholesterol, and triacylglycerol concentrations decreased (P < 0.01) by 21 ± 4%, 25 ± 10%, and 32 ± 6%, respectively, after 8 wk of ADF, whereas HDL cholesterol remained unchanged. Systolic blood pressure decreased (P < 0.05) from 124 ± 5 to 116 ± 3 mm Hg.

Conclusion: These findings suggest that ADF is a viable diet option to help obese individuals lose weight and decrease CAD risk. This trial was registered at clinicaltrials.gov as UIC-004-2009.

Circadian Timing of Food Intake Contributes to Weight Gain

Circadian Timing of Food Intake Contributes to Weight Gain

Deanna M. Arble1, Joseph Bass1,2, Aaron D. Laposky1, Martha H. Vitaterna1 and Fred W. Turek1

Abstract

Studies of body weight regulation have focused almost entirely on caloric intake and energy expenditure. However, a number of recent studies in animals linking energy regulation and the circadian clock at the molecular, physiological, and behavioral levels raise the possibility that the timing of food intake itself may play a significant role in weight gain. The present study focused on the role of the circadian phase of food consumption in weight gain. We provide evidence that nocturnal mice fed a high-fat diet only during the 12-h light phase gain significantly more weight than mice fed only during the 12-h dark phase. A better understanding of the role of the circadian system for weight gain could have important implications for developing new therapeutic strategies for combating the obesity epidemic facing the human population today.

A very low carbohydrate ketogenic diet improves glucose tolerance in ob/ob mice independently of weight loss

A very low carbohydrate ketogenic diet improves glucose tolerance in ob/ob mice independently of weight loss

by Badman, M. K., Kennedy, A. R., Adams, A. C., Pissios, P., Maratos-Flier, E.

In mice of normal weight and with diet-induced obesity, a high-fat, low-carbohydrate ketogenic diet (KD) causes weight loss, reduced circulating glucose and lipids, and dramatic changes in hepatic gene expression. Many of the effects of KD are mediated by fibroblast growth factor 21 (FGF21). We tested the effects of KD feeding on ob/ob mice to determine if metabolic effects would occur in obesity secondarily to leptin deficiency. We evaluated the effect of prolonged KD feeding on weight, energy homeostasis, circulating metabolites, glucose homeostasis, and gene expression. Subsequently, we evaluated the effects of leptin and fasting on FGF21 expression in ob/ob mice. KD feeding of ob/ob mice normalized fasting glycemia and substantially reduced insulin and lipid levels in the absence of weight loss. KD feeding was associated with significant increases in lipid oxidative genes and reduced expression of lipid synthetic genes, including stearoyl-coenzyme A desaturase 1, but no change in expression of inflammatory markers. In chow-fed ob/ob mice, FGF21 mRNA was elevated 10-fold compared with wild-type animals, and no increase from this elevated baseline was seen with KD feeding. Administration of leptin to chow-fed ob/ob mice led to a 24-fold induction of FGF21. Fasting also induced hepatic FGF21 in ob/ob mice. Thus, KD feeding improved ob/ob mouse glucose homeostasis without weight loss or altered caloric intake. These data demonstrate that manipulation of dietary macronutrient composition can lead to marked improvements in metabolic profile of leptin-deficient obese mice in the absence of weight loss.

Inflammation and impaired adipogenesis in hypertrophic obesity in man

Inflammation and impaired adipogenesis in hypertrophic obesity in man

by Gustafson, B., Gogg, S., Hedjazifar, S., Jenndahl, L., Hammarstedt, A., Smith, U.

Obesity is associated mainly with adipose cell enlargement in adult man (hypertrophic obesity), whereas the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of body mass index, is negatively correlated with whole body insulin sensitivity. Here, we review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue, including local cellular insulin resistance with reduced IRS-1 and GLUT4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation, a well-known finding in these individuals and one that promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNF, but not MCP-1, resistin, or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling, and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications.

The origin of intermuscular adipose tissue and its pathophysiological implications

The origin of intermuscular adipose tissue and its pathophysiological implications

by Vettor, R., Milan, G., Franzin, C., Sanna, M., De Coppi, P., Rizzuto, R., Federspil, G.

The intermuscular adipose tissue (IMAT) is a depot of adipocytes located between muscle bundles. Several investigations have recently been carried out to define the phenotype, the functional characteristics, and the origin of the adipocytes present in this depot. Among the different mechanisms that could be responsible for the accumulation of fat in this site, the dysdifferentiation of muscle-derived stem cells or other mesenchymal progenitors has been postulated, turning them into cells with an adipocyte phenotype. In particular, muscle satellite cells (SCs), a heterogeneous stem cell population characterized by plasticity and self-renewal that allow muscular growth and regeneration, can acquire features of adipocytes, including the abilities to express adipocyte-specific genes and accumulate lipids. Failure to express the transcription factors that direct mesenchymal precursors into fully differentiated functionally specialized cells may be responsible for their phenotypic switch into the adipogenic lineage. We proved that human SCs also possess a clear adipogenic potential that could explain the presence of mature adipocytes within skeletal muscle. This occurs under some pathological conditions (i.e., primary myodystrophies, obesity, hyperglycemia, high plasma free fatty acids, hypoxia, etc.) or as a consequence of thiazolidinedione treatment or simply because of a sedentary lifestyle or during aging. Several pathways and factors (PPARs, WNT growth factors, myokines, GEF-GAP-Rho, p66shc, mitochondrial ROS production, PKCß) could be implicated in the adipogenic conversion of SCs. The understanding of the molecular pathways that regulate muscle-to-fat conversion and SC behavior could explain the increase in IMAT depots that characterize many metabolic diseases and age-related sarcopenia.

Transdifferentiation properties of adipocytes in the adipose organ

Transdifferentiation properties of adipocytes in the adipose organ

by Cinti, S.

Mammals have two types of adipocytes, white and brown, but their anatomy and physiology is different. White adipocytes store lipids, and brown adipocytes burn them to produce heat. Previous descriptions implied their localization in distinct sites, but we demonstrated that they are mixed in many depots, raising the concept of adipose organ. We explain the reason for their cohabitation with the hypothesis of reversible physiological transdifferentiation; they are able to convert one into each other. If needed, the brown component of the organ could increase at the expense of the white component and vice versa. This plasticity is important because the brown phenotype of the organ associates with resistance to obesity and related disorders. Another example of physiological transdifferetiation of adipocytes is offered by the mammary gland; the pregnancy hormonal stimuli seems to trigger a reversible transdifferentiation of adipocytes into milk-secreting epithelial glands. The obese adipose organ is infiltrated by macrophages inducing chronic inflamation that is widely considered as a causative factor for insulin resistance. We showed that the vast majority of macrophages infiltrating the obese organ are arranged around dead adipocytes, forming characteristic crown-like structures. We recently found that visceral fat is more infiltrated than the subcutaneous fat despite a smaller size of visceral adipocytes. This suggests a different susceptibility of visceral and subcutaneous adipocytes to death, raising the concept of smaller critical death size that could be important to explain the key role of visceral fat for the metabolic disorders associated with obesity.

Exercise Training and Dietary Glycemic Load May Have Synergistic Effects on Insulin Resistance in Older Obese Adults

Exercise Training and Dietary Glycemic Load May Have Synergistic Effects on Insulin Resistance in Older Obese Adults

John P. Kirwana-d, Hope Barkoukisd, Latina M. Brooksa, b, Christine M. Marchettie, Bradley P. Stetzere, Frank Gonzalezf

  Abstract

Background/Aims: The aim of this study was to assess the combined effects of exercise and dietary glycemic load on insulin resistance in older obese adults. Methods: Eleven men and women (62 ± 2 years; 97.6 ± 4.8 kg; body mass index 33.2 ± 2.0) participated in a 12-week supervised exercise program, 5 days/week, for about 1 h/day, at 80-85% of maximum heart rate. Dietary glycemic load was calculated from dietary intake records. Insulin resistance was determined using the euglycemic (5.0 mM) hyperinsulinemic (40 mU/m2/min) clamp. Results: The intervention improved insulin sensitivity (2.37 ± 0.37 to 3.28 ± 0.52 mg/kg/min, p < 0.004), increased VO2max (p < 0.009), and decreased body weight (p < 0.009). Despite similar caloric intakes (1,816 ± 128 vs. 1,610 ± 100 kcal/day), dietary glycemic load trended towards a decrease during the study (140 ± 10 g before, vs. 115 ± 8 g during, p < 0.04). The change in insulin sensitivity correlated with the change in glycemic load (r = 0.84, p < 0.009). Four subjects reduced their glycemic load by 61 ± 8%, and had significantly greater increases in insulin sensitivity (78 ± 11 vs. 23 ± 8%, p < 0.003), and decreases in body weight (p < 0.004) and plasma triglycerides (p < 0.04) compared to the rest of the group. Conclusion: The data suggest that combining a low-glycemic diet with exercise may provide an alternative and more effective treatment for insulin resistance in older obese adults.

Effects of apple juice on risk factors of lipid profile, inflammation and coagulation, endothelial markers and atherosclerothic lesions in highcholesterolemic rabbits

Effects of apple juice on risk factors of lipid profile, inflammation and coagulation, endothelial markers and atherosclerothic lesions in highcholesterolemic rabbits

by Nafiseh Esmaeil

Background: Atherosclerosis which results from gradual deposition of lipids in medium and large arteries is a leading cause of mortality worldwide. The objective of this study was to determine the effect of apple juice on some risk factors of atherosclerosis and on the development of atherosclerosis in rabbits fed a high-cholesterol diet. Methods: Thirty two male rabbits were randomly divided into four groups: normal diet, high cholesterol diet (%1 cholesterol), 1 % cholesterol supplemented with 5ml apple juice(low dose) and 1 % cholesterol supplemented with 10ml apple juice (high dose) for 2 month. The C-reactive protein (CRP), nitrite, nitrate, fibrinogen,total cholesterol(TC) and factor VII were measured before the experiment and by the end of period. At the end ofstudy, fatty streak formation in right and left coronary arteries were determined using Chekanov method in all groups. Results: Both doses of apple juice significantly were decreased TC, TG, CRP, fibrinogen, factor VII levels, atherosclerotic lesion in right and left coronary arteries and increased nitrite and nitrate compared to cholesterolemic diet.Also using 10ml apple juice caused significant reduce in LDL-C and increase HDL-C , but 5 ml apple juice did not change these factors. Significant differences were observed between 5 and 10ml apple juice groups by LDL-C. No significant difference was found between 5 and 10 ml apple juice groups with regard to CRP, nitrite, nitrate, fibrinogen, factor VII, TG, HDL-C and TC concentrations. Conclusion: Apple juice can effectively prevent the progress of atherosclerosis.This is likely due to antioxidant and anti-inflammatory effect of apple juice.

Short-term effects of replacing milk with cola beverages on insulin-like growth factor-I and insulin-glucose metabolism: a 10 d interventional study in young men.

Short-term effects of replacing milk with cola beverages on insulin-like growth factor-I and insulin-glucose metabolism: a 10 d interventional study in young men.

Hoppe C, Kristensen M, Boiesen M, Kudsk J, Fleischer Michaelsen K, Mølgaard C.

Department of Human Nutrition, University of Copenhagen, Rolighedsvej 30, DK-1958 Fredericksberg, Denmark.

In the Western world, a trend towards increased consumption of carbonated soft drinks combined with a decreasing intake of milk is observed. This may affect circulating insulin-like growth factor I (IGF-I) and fasting insulin, as seen in pre-pubertal children. The present study was designed to reflect the trend of replacing milk with carbonated beverages in young men and to study the effects of this replacement on IGF-I, IGF-binding protein 3 (IGFBP-3), IGF-I:IGFBP-3 and glucose-insulin metabolism. A randomised, controlled crossover intervention study, in which eleven men aged 22-29 years were given a low-Ca diet in two 10 d periods with 10 d washout in between. In one period, they drank 2.5 litres of Coca Cola(R) per day and the other period 2.5 litres of semi-skimmed milk. Serum IGF-I, IGFBP-3 (RIA), insulin (fluoro immunoassay) and glucose (Cobas) were determined at baseline and end point of each intervention period. Insulin resistance and beta-cell function were calculated with the homeostasis model assessment. A decrease in serum IGF-I was observed in the cola period compared with the milk period (P < 0.05). No effects of treatment were observed on IGFBP-3, IGF-I:IGFBP-3, insulin, glucose, insulin resistance or beta-cell function. The present study demonstrates that high intake of cola over a 10 d period decreases total IGF-I compared with a high intake of milk, with no effect on glucose-insulin metabolism in adult men. It is unknown whether this is a transient phenomenon or whether it has long-term consequences.