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PubMed2005

Obesity-related cardiovascular risk factors: intervention recommendations to decrease adolescent obesity.

The incidence of adolescent obesity is increasing dramatically in the United States with associated risks of hypertension, adverse lipid profiles, and Type II diabetes. Unless reversed, this trend predicts an epidemic of adult cardiovascular disease. Interventions at home, at school, and in the community are required to empower teens to increase physical activity and to modify eating habits. This article describes assessment for obesity-related health problems as well as scientific guidelines and research-based intervention strategies to decrease obesity in adolescents.

Adolescent↗
PubMed2003

Diet-dependent obesity and hypercholesterolemia in the New Zealand obese mouse: identification of a quantitative trait locus for elevated serum cholesterol on the distal mouse chromosome 5.

AIMS: New Zealand obese (NZO) mice exhibit a polygenic syndrome of obesity, insulin resistance, and hypercholesterolemia that resembles the human metabolic syndrome. This study was performed in order to locate genes responsible for elevated serum cholesterol and to compare their effects under a standard and high fat diet. METHODS: A backcross population of NZO with SJL mice (NZO x F1(SJL x NZO)) was generated. Mice were raised on a normal or high fat diet and were monitored for 22 weeks (body weight, serum cholesterol, and blood glucose). A genome-wide scan was performed by genotyping of approximately 200 polymorphic microsatellite markers by PCR and linkage analysis was performed with the MAPMAKER program. RESULTS: In the genome-wide scan, a single susceptibility locus for hypercholesterolemia (Chol1/NZO, maximum LOD score 14.5 in a combined population of 523 backcross mice) was identified on chromosome 5. Cholesterol levels were significantly elevated in both male and female homozygous carriers of the Chol1/NZO allele. The locus maps 40cM distal of the previously described obesity locus Nob1 in the vicinity of the marker D5Mit244 and in the vicinity of hypercholesterolemia QTL previously identified in the NZB, CAST, and C57BL/6J strains. Chol1/NZO was not associated with elevated body weight, serum insulin, or hyperglycemia. The high fat diet significantly increased serum cholesterol levels, but the fat content of the diet did not alter the absolute effect of Chol1/NZO. CONCLUSIONS: Chol1/NZO is a major susceptibility locus on the distal mouse chromosome 5, which produces gender-independent hypercholesterolemia in NZO mice. The effect of Chol1/NZO was independent of the dietary fat content and was not associated with the other traits of the metabolic syndrome. Thus, it is suggested that the responsible gene might be involved in cholesterol metabolism.

Animals↗
PubMed2002

Characterization of diet-induced obese rats that develop persistent obesity after 6 months of high-fat followed by 1 month of low-fat diet.

A subset of Sprague-Dawley rats developed persistent obesity when maintained on a high-fat diet for 6 months followed by a low-fat diet for 1 month, while another subset from the same cohort of rats remained lean on the same diet regimens. The diet-induced obese (DIO) rats had higher energy intake than expenditure, while diet-resistant (DR) rats maintained energy balance. DIO rats also had an increased respiratory quotient and higher levels of plasma leptin, insulin and cholesterol. In the hypothalamic areas, DIO rats had elevated NPY and AGRP mRNA, but not MCH mRNA. Our data suggest that the increase in hypothalamic expression of NPY and AGRP may contribute to the development of persistent obesity in DIO rats.

Agouti-Related Protein↗
PubMed1986

Differential effect of common snack foods on caloric intake, growth and obesity in weanling male and female rats with hypothalamic obesity.

In order to see whether weanling normophagic rats with hypothalamic obesity (VMNL rats) become hyperphagic and more obese than when fed lab chow, and to see in addition whether there is a possible sex difference in whatever response is found, male and female VMNL rats were fed lab chow for 14 days after lesion production and then, for the following 42 days, they received Hostess HoHos, potato chips, marshmallows and french fries in addition to lab chow. At termination, body weights were similar among the groups, but VMNL rats were fatter and shorter than controls. Also, female VMNL rats were fatter and shorter than male VMNL rats and layed down more fat per unit of food energy. Total caloric intake was greater in controls than in VMNL rats and in males than in females. However, the females showed a decrease in intake and the males an increase over time. Males ate more lab chow and french fries than females. Lab chow was the only food that VMNL rats ate more of than controls. The VMNL rats ate less french fries, HoHos and potato chips than controls, but similar amounts of marshmallows. There was no sex difference in macronutrient intake and per cent macronutrient intake. Moreover, controls ate as much carbohydrate and less per cent carbohydrate than VMNL rats, more fat than VMNL rats, but normal per cent fat and normal protein and per cent protein. Sex X lesion interactions indicated that female VMNL rats ate more per cent carbohydrate than female controls and male VMNL rats, ate more protein than male controls. The greater degree of obesity in the females despite the lower caloric intake may be due to enhanced food energy utilization. The data also show that weanling VMNL rats do not exhibit the great preference for palatable diets that have been reported for mature rats with ventromedial hypothalamic area lesions and that the only sex difference in intake is with french fries, which have neither the highest fat nor the highest carbohydrate content of the foods tested.

Animals↗
PubMed1981

Levels of gastrin-cholecystokinin-like immunoreactivity in the brains of genetically obese and non-obese rats.

Levels of gastrin-cholecystokinin-like immunoreactivity were measured in three brain regions (cortex, diencephalon, brainstem) and the pituitary gland in groups of genetically obese Zucker rats and their non-obese littermates. The obese animals had significantly increased body weights and significantly lowered brain weights. However, levels of gastrin-cholecystokinin-like immunoreactivity were not different between the two groups in any of the regions measured. These results contrast with a recent report [11] in which ob/ob mice were found to have decreased levels of cholecystokinin in their brains.

Animals↗
PubMed2003

The metabolic syndrome as a vicious cycle: does obesity beget obesity?

Most attempts at weight loss are frustrated by the body's propensity to maintain fat mass. There are genetic and environmental mechanisms behind this phenomenon, such as thrifty genes, sedentary lifestyle and abundant food resources. We will outline a physiologic mechanism that may perpetuate obesity once it develops. Specifically, we suggest that obesity-induced hyperinsulinemia facilitates fuel storage as fat. This can be exacerbated by high glucocorticoid activity, low growth hormone (GH) activity and the paradoxical increase in free fatty acid (FFA) flux resulting from basal lipolysis in an expanded fat mass. We also outline mechanisms by which obesity may perpetuate low GH and increased glucocorticoid activity in the metabolic syndrome.

Fatty Acids↗
PubMed2002

Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance.

Insulin signaling in adipose tissue plays an important role in lipid storage and regulation of glucose homeostasis. Using the Cre-loxP system, we created mice with fat-specific disruption of the insulin receptor gene (FIRKO mice). These mice have low fat mass, loss of the normal relationship between plasma leptin and body weight, and are protected against age-related and hypothalamic lesion-induced obesity, and obesity-related glucose intolerance. FIRKO mice also exhibit polarization of adipocytes into populations of large and small cells, which differ in expression of fatty acid synthase, C/EBP alpha, and SREBP-1. Thus, insulin signaling in adipocytes is critical for development of obesity and its associated metabolic abnormalities, and abrogation of insulin signaling in fat unmasks a heterogeneity in adipocyte response in terms of gene expression and triglyceride storage.

Adipocytes↗
PubMed2000

Weight loss, weight maintenance, and improved cardiovascular risk factors after 2 years treatment with orlistat for obesity. European Orlistat Obesity Study Group.

OBJECTIVE: To determine the effect of orlistat, a new lipase inhibitor, on long-term weight loss, to determine the extent to which orlistat treatment minimizes weight regain in a second year of treatment, and to assess the effects of orlistat on obesity-related risk factors. RESEARCH METHODS AND PROCEDURES: This was a 2-year, multicenter, randomized, double-blind, placebo-controlled study. Obese patients (body mass index 28 to 43 kg/m2) were randomized to placebo or orlistat (60 or 120 mg) three times a day, combined with a hypocaloric diet during the first year and a weight maintenance diet in the second year of treatment to prevent weight regain. Changes in body weight, lipid profile, glycemic control, blood pressure, quality of life, safety, and tolerability were measured. RESULTS: Orlistat-treated patients lost significantly more weight (p<0.001) than placebo-treated patients after Year 1 (6.6%, 8.6%, and 9.7% for the placebo, and orlistat 60 mg and 120 mg groups, respectively). During the second year, orlistat therapy produced less weight regain than placebo (p = 0.005 for orlistat 60 mg; p<0.001 for orlistat 120 mg). Several obesity-related risk factors improved significantly more with orlistat treatment than with placebo. Orlistat was generally well tolerated and only 6% of orlistat-treated patients withdrew because of adverse events. Orlistat leads to predictable gastrointestinal effects related to its mode of action, which were generally mild, transient, and self-limiting and usually occurred early during treatment. DISCUSSION: Orlistat administered for 2 years promotes weight loss and minimizes weight regain. Additionally, orlistat therapy improves lipid profile, blood pressure, and quality of life.

Adult↗
PubMed1997

Weight development, drop-out pattern and changes in obesity-related risk factors after two years treatment of obese men.

OBJECTIVE: To describe a combined behavioural treatment program for obese men, the 'Gustaf' study, and to evaluate treatment success by the means of weight loss, drop-out analysis and changes in metabolic risk factors. SUBJECTS: Eighty-six men, aged 43 +/- 9 y (mean +/- s.d.) and BMI 37.7 +/- 4.4 kg/m2, from the waiting list of the outpatient clinic and men directly approaching the Obesity Unit. DESIGN: Combined, behavioural modification treatment, by the means of group sessions, for one hour every week over a two year period. MAIN OUTCOME MEASURES: Weight loss and changes in risk factors after completion of one and two years study and description of treatment success in the form of changes in metabolic risk factors. RESULTS: The one year drop-out rate was 22% and the cumulative rate after two years was 34%. Mean weight decreased significantly from start (121 kg) to one year (114 kg, P < 0.001) and to two years (115 kg, P < 0.001) in completers. Several metabolic risk factors (waist and hip circumferences, systolic blood pressure, serum cholesterol and plasma insulin) remained significantly decreased after two years of treatment. The complete metabolic syndrome was diagnosed in five men at onset, but in no one after two years. There was no difference in change of metabolic risk factors after one year between the men who lost 8-12% of initial body weight and those who lost more. CONCLUSION: Sixty-six% (57/86) of the obese men who started in the 'Gustaf' program were still in the program after two years. In spite of the relatively modest weight loss, the men maintained a large proportion of this weight loss and also maintained their improved metabolic risk factor pattern.

Adult↗
PubMed2000

Psychometric properties and factor structure of the Three-Factor Eating Questionnaire (TFEQ) in obese men and women. Results from the Swedish Obese Subjects (SOS) study.

OBJECTIVE: To evaluate the construct validity of the Three-Factor Eating Questionnaire (TFEQ) in obese men and women. SUBJECTS: A total of 4377 middle-aged, obese subjects in the Swedish Obese Subjects (SOS) study. METHODS: The total sample was randomly split into two data subsets and psychometric testing was performed separately in each sample. Multitrait/multi-item analysis was conducted to test scaling assumptions and factor analysis was used to test the factor structure. Measures of mental well-being (MACL, HAD) were used for testing criterion-based validity. RESULTS: The Cognitive Restraint factor was consistently reproduced and scaling analysis demonstrated strong item-scale discriminant validity, while the item-scale convergent validity was unsatisfactory. The internal structure of the Disinhibition scale was weak. Most Disinhibition and Hunger items grouped in one global factor labeled Uncontrolled Eating. A third cluster containing items on Emotional Eating was also identified. The obtained three-factor structure was cross-validated and replicated across subgroups by gender, age and BMI. CONCLUSION: The original TFEQ factor structure was not replicated. A short, revised 18-item instrument was constructed, representing the derived factors of Cognitive Restraint, Uncontrolled Eating and Emotional Eating. The most efficient items were used to boost both the convergent and discriminant validity of the scales.

Adult↗
PubMed2002

Habitual fat intake and basal fat oxidation in obese and non-obese Caucasians.

OBJECTIVE: To examine the relationship between habitual fat intake and basal fat oxidation in obese and non-obese Caucasian men and women. METHODS: Habitual fat intake was assessed by 7-day weighed dietary records and resting fat oxidation was determined after an overnight fast in 132 weight stable non-diabetic subjects (38 males, 94 females). All subjects were characterized for weight, height, waist-to-hip ratio, physical activity, plasma glucose and insulin response to an oral glucose load, plasma catecholamine and leptin levels. Under-reporters, defined according to plausibility of the relationship between energy expenditure and energy intake, were excluded from the analyses. RESULTS: The mean age was 53.1+/-10.6 y (19-72 y) and mean body mass index (BMI) was 30.7+/-5.8 kg/m(2) (19.4-45.8 kg/m(2)). Sixty-eight subjects were obese (BMI>30 kg/m(2)). Univariate regression analysis revealed a significant, albeit modest, relationship between absolute fat intake and BMI (r(2)=0.06; P<or=0.05) but not between fat intake and fat mass (r(2)=0.026; P=0.08). However, multiple regression analysis revealed significant effects of body fat mass (FM) and sex on basal fat oxidation (bFO) explaining 33% of the variation of bFO (P<or=0.0001; radical s.e.=18.0 g/24 h). In univariate regression analysis, habitual fat intake was significantly related to adjusted fat oxidation, explaining 12% of the variation (P<or=0.0001; radical s.e.=11.7 g/24 h). CONCLUSION: Habitual fat intake has a significant, albeit modest, effect on basal fat oxidation, even when adjusted for sex and body FM. The rather modest effect of habitual fat intake on fat oxidation may in part explain the increased propensity to gain FM on a high-fat diet.

Adult↗
PubMed2002

Obesity, atherosclerosis and the vascular endothelium: mechanisms of reduced nitric oxide bioavailability in obese humans.

It is now well established that obesity is an independent risk factor for the development of coronary artery atherosclerosis. The maintenance of vascular homeostasis is critically dependent on the continued integrity of vascular endothelial cell function. A key early event in the development of atherosclerosis is thought to be endothelial cell dysfunction. A primary feature of endothelial cell dysfunction is the reduced bioavailability of the signalling molecule nitric oxide (NO), which has important anti atherogenic properties. Recent studies have produced persuasive evidence showing the presence of endothelial dysfunction in obese humans NO bioavailability is dependent on the balance between its production by a family of enzymes, the nitric oxide synthases, and its reaction with reactive oxygen species. The endothelial isoform (eNOS) is responsible for a significant amount of the NO produced in the vascular wall. NO production can be modulated in both physiological and pathophysiological settings, by regulation of the activity of eNOS at a transcriptional and post-transcriptional level, by substrate and co-factor provision and through calcium dependent and independent signalling pathways. The present review discusses general mechanisms of reduced NO bioavailability including factors determining production of both NO and reactive oxygen species. We then focus on the potential factors responsible for endothelial dysfunction in obesity and possible therapeutic interventions targetted at these abnormalities.

Arteriosclerosis↗
PubMed2001

Metabolic changes following sibutramine-assisted weight loss in obese individuals: role of plasma free fatty acids in the insulin resistance of obesity.

The relationship between insulin-mediated glucose disposal and daylong free fatty acid (FFA) concentrations before and after sibutramine-assisted weight loss was investigated in 24 healthy, normotensive, nondiabetic, obese women (body mass index [BMI] >30.0 kg/m(2)). The 24 volunteers were defined as being insulin-resistant (IR) or insulin-sensitive (IS) on the basis of their steady-state plasma glucose (SSPG) concentration in response to a 180-minute continuous intravenous infusion of octreotide, insulin, and glucose. The mean (+/- SEM) SSPG concentrations were significantly higher (P <.001) in the IR group (219 +/- 7 v 69 +/- 6 mg/dL) at baseline. The IR group also had significantly higher plasma glucose (P =.002), insulin (P <.001), and FFA (P =.02) concentrations measured at hourly intervals from 8 AM to 4 PM, before and after breakfast (8 AM) and lunch (noon). Weight loss in response to an energy-restricted diet for 4 months and sibutramine (15 mg/d) was comparable in the 2 experimental groups (8.6 +/- 1.3 v 7.9 +/- 1.4 kg). SSPG concentrations decreased significantly (P <.001) following weight loss (219 +/- 7 to 144 +/- mg/dL) in the IR group, but there was no change in the SSPG of the IS group (69 +/- 6 to 73 +/- 7 mg/dL. The improvement in insulin sensitivity in the IR group after weight loss was associated with a significant decline in daylong plasma glucose (P >.001) and insulin (P =.02) concentrations, without a weight-loss-associated decrease in daylong plasma FFA responses. In contrast, there was no significant change in plasma glucose, insulin, and FFA concentrations following weight loss in the IS group. These results indicate that daylong FFA concentrations vary substantially in obese individuals as a function of whether they are IR or IS. Furthermore the observation that the IR group was more insulin-sensitive after weight loss, associated with lower daylong insulin concentrations in the absence of a significant decrease in circulating FFA concentrations, suggests that resistance to insulin-mediated glucose disposal in obese individuals cannot be entirely due to high FFA levels.

Adipose Tissue↗
PubMed1986

Serum somatomedin activity and growth hormone level in obese men: dependence on degree of obesity and hyperlipidemia.

The effect of body weight excess and hyperlipidemia on stimulated growth hormone (GH) secretion and serum somatomedin activity (SSA) has been investigated. Among 40 obese men gradually impairment of GH secretory response during the insulin hypoglycemia test was shown. Propranolol-L-DOPA administration elicited satisfactory GH secretory response only in the subgroup of patients with the mild weight excess. SSA was found to be in the normal range among the whole group of obese patients, however, it was significantly depressed in subjects with average weight excess higher than 100%. Obese men with hypertriglyceridemia and hypercholesterolemia presented low SSA even when their weight excess was relatively moderate, i.e., 52% and 57%, respectively.

Adult↗
PubMed1976

Childhood antecedents of adult obesity. Do chubby infants become obese adults?

We investigated whether obese infants tend to become obese adults. Records of subjects born between 1945 and 1955 were reviewed to select three cohorts based on weight in the first six months of age, which exceeded the 90th percentile at least once, ranged between 25th and 75th percentiles or was below 10th percentile at least once. Three hundred and sixty-six subjects, now between 20 and 30 years of age, were located and their present height and weight determined. Thirty-six per cent of those exceeding the 90th percentile as infants were overweight adults, as compared to 14 per cent of the average age and light-weight infants. A significant increase (chi square = 17.2, p less than 0.001) in adult obesity was evident when the infant exceeded the 75th percentile that was independent of his height. Social class, educational level, and parental weight all correlated with adult weight (p less than 0.001). Sex and ordinal position of birth did not. The data suggest that infant weight correlates strongly with adult weight independently of other factors considered.

Adolescent↗
PubMed2005

The global obesity epidemic: snacking and obesity may start with free meals during infant feeding.

UNLABELLED: Feeding is vital for survival. The brain has strong hunger and reward mechanisms that ensure optimal food intake for adequate nutrition. The drive for feeding is particularly strong in humans whose large brains require large energy support. This starts immediately after birth; the newborn child being able to taste sucrose and suck the sweet and fat from its mother's milk. At present, mothers are generally advised to breastfeed children as often as they like, which may be up to 15 times a day. At the same time, childhood obesity is rapidly developing. One reason for the rapidly increasing prevalence of childhood obesity may be overfeeding with snack food. CONCLUSION: We hypothesize that non-rule breastfeeding favours the development of snacking throughout the day during childhood, a habit which in turn favours the development of obesity.

Appetite Regulation↗
PubMed1978

Protein utilization and lysine metabolism in obese and non-obese growing rats.

Efficiency of protein utilization and lysine metabolism were studied in growing rats of the Zucker 13M strain, both obese and lean, and in the Charles River CD strain. When graded levels of wheat gluten or wheat gluten supplemented with lysine were fed to these three types of rats, no significant differences in the efficiency of protein utilization were found. However, under these dietary conditions, the Zucker obese rats appeared to be about 167% more efficient in energy utilization than the Zucker lean rats or the Charles River strain. The response of liver lysine-ketoglutarate reductase to the dietary treatment was similar in these three types of growing rats. The enzyme activity was induced by dietary lysine. Rats fed a lysine-deficient purified diet had a significantly lower enzyme activity than those fed a protein-free diet indicating that the same adaptive mechanism for lysine conservation as previously observed in adult rats also occurred in the growing animal. Interaction between dietary and genetic factors on fatty liver was found in this study. The most severe fatty liver was observed in the Zucker obese rats fed the most lysine-deficient diet containing 8% wheat gluten protein.

Animals↗
PubMed1993

Effects of alcohol intake and obesity on serum liver enzyme activity in obese men with mild hypertension.

OBJECTIVES: To examine the relationships between alcohol intake, obesity, plasma insulin concentration and serum activities of three liver enzymes in obese men with mild hypertension. DESIGN: A 6-week run-in period followed by randomization to either diet treatment or antihypertensive drug treatment, lasting for 1 year. Alcohol intake was estimated using questionnaires. Plasma insulin concentration, serum activities of gamma-glutamyl transferase, and aspartate and alanine aminotransferase, respectively, were measured at entry and after 1 year. SETTING: Out-patient clinic, city hospital. PATIENTS: Sixty-four men aged 40-69 years with a body mass index > or = 26 kg m-1 and with mild untreated hypertension. Exclusion criteria were alcoholism and diabetes mellitus. Sixty-one patients completed the study. INTERVENTIONS: Dietary treatment was based upon weight reduction and recommendations about a low alcohol intake. Drug treatment used a stepped-care approach with atenolol as the first-choice drug. MAIN OUTCOME MEASURES: Serum activities of the liver enzymes, body weight, body mass index, alcohol intake, plasma insulin concentration. RESULTS: Body weight decreased by 7.8 kg in the diet group and increased by 1.0 kg in the drug-treated group. Alcohol intake did not differ between the groups before or after 1 year. Serum gamma-glutamyl transferase activity correlated with alcohol consumption; it showed no significant change after weight loss. At entry, serum activities of aspartate and alanine aminotransferases correlated to plasma insulin concentration independent of body mass index. Weight reduction significantly lowered serum activities of these liver enzymes as well as plasma insulin concentrations and normalized elevated serum activity of alanine aminotransferase in a majority of the cases. CONCLUSION: Alcohol intake was an important determinant for elevated serum gamma-glutamyl transferase activity. The degree of obesity was a contributing factor for elevations of serum alanine aminotransferase activity. We speculate that insulin may play a role in this relationship.

Adult↗