Eating behaviors in adolescent Egyptian girls

The present cross-sectional study was designed to assess the prevalence of disordered eating attitudes and behaviors in school-based girls in Cairo, in which a modified Eating Attitudes Test was used. Documenting the development of dieting preoccupation in young children may help with early identification and perhaps lead to intervention strategies. The study included 137 student girls [age range 12-17 years]: first group, [54] with age range 12-14 years and a mean age of 13.1 +/- 1.2 years and second group, [83] with age range 15-17 years and a mean age of 16.2 +/- 0.8 years group. Only 1.5% of the students scored >/= 20 on the ChEAT, which is the cut-off score for anorexia nervosa for the EAT-26. These were all in the 15-17 years old group, 2.4% scored >/= 20. The overall mean ChEAT score was more in the second older group 10.2 +/- 4.9 with a range of 3 to 28 compared to the first younger group 5.9 +/- 2.6 with a range of 2 to 12 [p<0.001]. We have no scores in both groups in the item "Eat diet food" and "Have the impulse to vomit after meals". Girls in the second group were more "scared about being overweight", "Preoccupied with a desire to be thinner", "Engaged in dieting behavior" and "Feel that food control there life"; whereas girls in the first group were more claimed that "others would like them to eat more" and "others think that they are too thin"

Fat cell size: obesity and growth hormone deficiency

Adipose tissue is a specialized connective tissue that functions as the major storage site for fat in the form of triglycerides. The size of adipose tissue mass is a function of both adipocyte number and size. Eighteen prepubertal obese children aged 10-13 years, fourteen GH deficient children aged 8-14 years, and thirty lean healthy children aged 9-13 years were included in the study. All obese children had a body mass index [BMI] above +3 SDS for age. Abdominal subcutaneous adipose tissue samples [100-300mg] were removed and adipocytes were isolated. The adipocyte diameter of 100 cells from each individual was measured under direct microscope and adipocyte size was calculated. Adipocyte volume was larger in obese children 713 +/- 113 p1 than in normal control children 121 +/- 11 p1 [p<0.001]. Adipocyte volume was larger in GH deficient children 441 +/- 87 p1 than in lean healthy control children 121 +/- 11 p1 [p<0.01]. Moreover, adipocyte volume was larger in obese children than in GH deficient children [p<0.05]. The average size and lipid content of subcutaneous adipocytes in GH-deficient patients and obese children is greater than in normal subjects. In conclusion, we found that fat cell size was larger in GH deficient children and obese children than in lean healthy children

Lipogenesis in non-insulin-dependent diabetes mellitus in GK rats

Non-insulin dependent diabetes mellitus [T2DM] now accounts for a considerable proportion of newly diagnosed cases of diabetes. Increasing rates of T2DM among children and adolescents will have considerable long-term implications for the affected individuals, society, and the public health system as a whole. The study comprised 6 male normal Fischer rats and 9 diabetic GK rats. Adipocytes were isolated, male rats [75 days] were decapitated after carbon dioxide anaesthasia, and the epididymal fat depots [1-2 g] were removed. Lipogenesis was determined by glucose incorporation into lipids at low glucose concentrations [1 micro mol/L] where glucose transport is rate-limiting. The basal lipogenesis was 1.25 +/- 0.3 nmol glucose incorporated into lipids/g in adipocytes of normal Fischer rats and 0.45 +/- 0.2 nmol glucose incorporated into lipids/g in adipocytes of diabetic GK rats [P<0.001, Fig 1]. The maximum insulin-induced lipogenesis was 6.2 +/- 0.1 nmol glucose incorporated into lipids/g in adipocytes of normal Fischer rats and 2.1 +/- 0.2 nmol glucose incorporated into lipids/g in adipocytes of diabetic GK rats [P<0.0001, Fig. 2]. The insulin sensitivity, expressed as EC50, did not vary between adipocytes of normal Fischer rats and diabetic GK rats. In conclusion, we found that both basal lipogenesis and maximum insulin-induced lipogenesis were higher in normal Fischer rats than in diabetic GK rats. Variation in lipogenesis may be of importance in understanding the mechanism of insulin resistance in Type II Diabetes Mellitus