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Objectives: To investigate the associations of dietary factors with overweight, body fat percentage (BF%), waist circumference (WC) and hip circumference (HC) among children. Design: Cross-sectional analysis of the Physical Activity and Nutrition in Children (PANIC) Study among 510 children (263 boys, 247 girls) aged 6–8 years from Kuopio, Finland. Methods: The children’s weight, height, WC and HC were measured. Overweight was defined by International Obesity Task Force body mass index cutoffs. The BF% was measured by dual-energy X-ray absorptiometry, nutrient intakes and meal frequency by 4-day food records and eating behaviour by Children’s Eating Behaviour Questionnaire. Results: Daily consumption of all the three main meals was inversely associated with overweight (odds ratio (OR) 0.37, 95% confidence interval (CI) 0.18–0.75), BF% ( β −0.12, P =0.012), WC ( β −0.16, P =0.002) and HC ( β −0.15, P =0.002). Enjoyment of food, food responsiveness and emotional overeating were directly associated with overweight (OR 1.57, 95% CI 1.04–2.35; OR 4.68, 95% CI 2.90–7.54; OR 2.60, 95% CI 1.52–4.45, respectively), BF% ( β 0.13, P =0.004; β 0.30, P <0.001; β 0.09, P =0.035, respectively), WC ( β 0.14, P =0.003; β 0.40, P <0.001; β 0.19, P <0.001, respectively) and HC ( β 0.15, P =0.001; β 0.38, P <0.001; β 0.15, P =0.001, respectively). Satiety responsiveness was inversely associated with overweight (OR 0.42, 95% CI 0.26–0.67), BF% ( β −0.20, P <0.001), WC ( β −0.26, P <0.001) and HC ( β −0.26, P <0.001). Slowness in eating was inversely associated with overweight (OR 0.61, 95% CI 0.41–0.92), WC ( β −0.16, P =0.001) and HC ( β −0.17, P <0.001). Protein intake was directly associated with BF% ( β 0.11, P =0.017), WC ( β 0.11, P =0.020) and HC ( β 0.13, P =0.008). Conclusions: Promoting regular consumption of main meals and healthy eating behaviours should be emphasized in the prevention of overweight among children. More research is needed on the association of protein-rich foods with body adiposity in children.

Objective: Lifestyle and genetic factors interact in the development of obesity and the metabolic syndrome. The molecular mechanisms underlying the beneficial dietary modifications are, however, unclear. We aimed to examine the effect of the long-term moderate weight reduction on gene expression in adipose tissue (AT) and to identify genes and gene clusters responsive to treatment and thereby likely contributing to the development of the metabolic syndrome. Design: Randomized controlled and individualized weight reduction intervention. Subjects: Forty-six subjects with impaired fasting glycemia or impaired glucose tolerance and features of metabolic syndrome, aged 60±7 years were randomized either to a weight reduction (WR) ( n =28) or a control ( n =18) group lasting for 33 weeks. Measurements: Oral and intravenous glucose tolerance tests and subcutaneous AT biopsies were performed before and after the intervention. Gene expression of AT was studied using microarray technology in subgroups of WR (with weight reduction ⩾5%, n =9) and control group ( n =10). The results were confirmed using quantitative PCR. Results: In the WR group, glucose metabolism improved. Moreover, an inverse correlation between the change in S I and the change in body weight was found ( r =−0.44, P =0.026). Downregulation of gene expression ( P <0.01) involving gene ontology groups of extracellular matrix and cell death was seen. Such changes did not occur in the control group. The tenomodulin-gene was one of the most downregulated genes (−39±16%, P <0.0001). Moreover, its expression correlated with insulin sensitivity ( r =−0.34, P =0.005) before the intervention and with body adiposity both before ( r =0.42, P =0.007) and after ( r =0.30, P =0.056) the intervention. Conclusion: Genes regulating the extracellular matrix and cell death showed a strong downregulation after long-term weight reduction. This likely reflects a new stable state at the molecular level in AT. Further studies are warranted to elucidate the mechanisms of these genetic factors.

Background/Objectives: To study nutrient intake, food consumption and meal pattern, and their associations with socioeconomic background in Finnish children. Subjects/Methods: The subjects were a population sample of 424 children (211 girls, 213 boys) 6–8 years of age. Nutrient intake and meal pattern were measured by food records, and food intake and socioeconomic characteristics were assessed by questionnaires. Results: Intakes of saturated fat, sucrose and salt were higher, and intakes of vitamin D, iron and fibre and unsaturated-to-saturated fat ratio lower than recommended. Less than 5% of children consumed vegetables, fruit and berries as recommended. Children with highest parental education more likely ate fish (odds ratio (OR) 2.20, 95% confidence interval (CI) 1.06–4.54), fibre-rich bread (OR 5.06, 95% CI 1.80–14.29) and main meals (OR 2.54, 95% CI 1.34–4.83), but less likely used soft margarine (OR 0.43, 95% CI 0.20–0.94) as recommended than children with lowest parental education. Children with highest household income more likely consumed skimmed milk (OR 2.43, 95% CI 1.21–4.88) and fish (OR 2.21, 95% CI 1.12–4.36) as recommended than children with lowest household income. Only 34% of girls and 45% of boys ate all main meals daily. Snacks provided as much as 42% of total energy intake. Conclusions: Children do not meet recommendations in all important nutrients. Children from lowest socioeconomic position least likely consumed fish, skimmed milk and fibre-rich bread and ate main meals, but most likely used soft margarine as recommended. Less than half of children ate all main meals daily.

Increased sedentariness has been linked to the growing prevalence of obesity in children, but some longitudinal studies suggest that sedentariness may be a consequence rather than a cause of increased adiposity. We used Mendelian randomization to examine the causal relations between body mass index (BMI) and objectively assessed sedentary time and physical activity in 3-8 year-old children from one Finnish and two Danish cohorts [NTOTAL =679]. A genetic risk score (GRS) comprised of 15 independent genetic variants associated with childhood BMI was used as the instrumental variable to test causal effects of BMI on sedentary time, total physical activity, and moderate-to-vigorous physical activity (MVPA). In fixed effects meta-analyses, the GRS was associated with 0.05 SD/allele increase in sedentary time (P=0.019), but there was no significant association with total physical activity (beta=0.011 SD/allele, P=0.58) or MVPA (beta=0.001 SD/allele, P=0.96), adjusting for age, sex, monitor wear-time and first three genome-wide principal components. In two-stage least squares regression analyses, each genetically instrumented one unit increase in BMI z-score increased sedentary time by 0.47 SD (P=0.072). Childhood BMI may have a causal influence on sedentary time but not on total physical activity or MVPA in young children. Our results provide important insights into the regulation of movement behaviour in childhood.

PURPOSE: Previous evidence for the associations of eating frequency and food consumption with clustering of metabolic risk factors among children is limited. We therefore investigated association of the daily number of main meals and snacks and food consumption with a metabolic risk score and individual metabolic risk factors in primary school children. METHODS: The subjects were a population sample of Finnish girls and boys 6–8 years of age. Dietary factors were measured by a four-day food record. Metabolic risk score was calculated summing up the Z-scores of waist circumference, systolic and diastolic blood pressure, and concentrations of fasting serum insulin and fasting plasma glucose, triglycerides and high-density lipoprotein cholesterol, the latest multiplying by −1. RESULTS: Skipping main meals (standardized regression coefficient β = −0.18, P < 0.001), a higher consumption of non-root vegetables (β = 0.18, P < 0.01), low-fat vegetable-oil-based margarine (β = 0.13, P < 0.01) and sugar-sweetened beverages (β = 0.11, P < 0.05) and a lower consumption of vegetable oils (β = −0.10, P < 0.05) were associated with a higher metabolic risk score after adjustment for age, sex, total physical activity, electronic media time, energy intake and other dietary factors. The consumption of red meat was directly related to the metabolic risk score, but the association was not statistically significant after adjustment for energy intake. CONCLUSIONS: Eating main meals regularly, decreasing the consumption of sugar-sweetened beverages and low-fat margarine and increasing the consumption of vegetable oils should be emphasized to reduce metabolic risk among children.

Background:Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.Participants and methods:A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).Results:Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8 ) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.Conclusions:We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

BACKGROUND AND OBJECTIVE: The short form (Glu9/Glu9) of the 12Glu9 deletion polymorphism of the alpha(2B)-adrenergic receptor gene was previously found to be associated with reduced basal metabolic rate in obese subjects. We investigated the effects of this polymorphism on changes in body weight in Finnish non-diabetic and type 2 diabetic subjects during a 10 y follow-up. DESIGN: Controlled 10 y follow-up study with baseline, 5 and 10 y examinations. SUBJECTS: A total of 126 non-diabetic control subjects and 84 newly diagnosed, middle-aged type 2 diabetic patients from eastern Finland participated. MEASUREMENTS: Anthropometric measurements, blood pressure, oral glucose tolerance test, plasma insulin, plasma C-peptide and glycosylated hemoglobin A(1C). Genotypes were determined by polymerase chain reaction followed by agarose gel electrophoresis. RESULTS: No significant differences were found in the prevalence of the 12Glu9 deletion polymorphism between non-diabetic and type 2 diabetic subjects. The non-diabetic subjects with the Glu9/Glu9 genotype had a greater increase in their mean body weight during 5 y follow-up than the non-diabetic subjects with other genotypes (changes in body weight 0.4+/-5.7, -0.5+/-6.4 and 3.4+/-4.9% for the Glu12/Glu12, Glu12/Glu9 and Glu9/Glu9 genotypes, respectively, P=0.040 for the difference between the groups). Also, the trend for the increment of body weight was statistically significant in the non-diabetic subjects with the Glu9/Glu9 genotype (P=0.012). The 12Glu9 polymorphism was not cross-sectionally or longitudinally associated with body weight in type 2 diabetic subjects. CONCLUSIONS: The genotype of two short alleles (Glu9/Glu9) was associated with an increase in body weight among non-diabetic subjects.

BACKGROUND AND OBJECTIVE:: The short form (Glu9 /Glu9 ) of the 12Glu9 deletion polymorphism of the [alpha]2B -adrenergic receptor gene was previously found to be associated with reduced basal metabolic rate in obese subjects. We investigated the effects of this polymorphism on changes in body weight in Finnish non-diabetic and type 2 diabetic subjects during a 10 y follow-up. DESIGN:: Controlled 10 y follow-up study with baseline, 5 and 10 y examinations. SUBJECTS:: A total of 126 non-diabetic control subjects and 84 newly diagnosed, middle-aged type 2 diabetic patients from eastern Finland participated. MEASUREMENTS:: Anthropometric measurements, blood pressure, oral glucose tolerance test, plasma insulin, plasma C-peptide and glycosylated hemoglobin A1c . Genotypes were determined by polymerase chain reaction followed by agarose gel electrophoresis. RESULTS:: No significant differences were found in the prevalence of the 12Glu9 deletion polymorphism between non-diabetic and type 2 diabetic subjects. The non-diabetic subjects with the Glu9 /Glu9 genotype had a greater increase in their mean body weight during 5 y follow-up than the non-diabetic subjects with other genotypes (changes in body weight 0.4±5.7, -0.5±6.4 and 3.4±4.9% for the Glu12 /Glu12 , Glu12 /Glu9 and Glu9 /Glu9 genotypes, respectively, P=0.040 for the difference between the groups). Also, the trend for the increment of body weight was statistically significant in the non-diabetic subjects with the Glu9 /Glu9 genotype (P=0.012). The 12Glu9 polymorphism was not cross-sectionally or longitudinally associated with body weight in type 2 diabetic subjects. CONCLUSIONS:: The genotype of two short alleles (Glu9 /Glu9 ) was associated with an increase in body weight among non-diabetic subjects. INTERNATIONAL JOURNAL OF OBESITY: (2001) 25, 1609-1614