Obesity as a poverty-related emerging nutrition problems: the case of Indonesia.

Obesity is a major contributor to the global burden of chronic disease and disability. In developing countries like Indonesia, obesity often co-exists with undernutrition. Data from national basic health research 2007 showed that overnutrition was found among all age groups, on a double digit scale, with similar magnitude in urban and rural areas and higher prevalence in adult female. In contrary to 14% undernourished children under the age of 5 years, 12% of their counterparts were overnourished; for 6-14 years 10% vs. 6%; and for 15 years and above 15% vs. 19%. The purpose of the review is to raise awareness on the increasing obesity problem and to set recommendations to prevent obesity. Stunted adults in developing countries are 1.2 times more likely to be overweight than non-stunted adults. Approaches to overcoming obesity in adulthood emphasize dietary changes, increasing physical activity and behaviour modification. It is important for Indonesia to target nutrition intervention for female adolescents, pregnant woman to first 2 years of life, initiate nutrition education for school-age children and disseminate Holistic Healthy Framework Approach with key message 'Initiate healthier food choices'. Prompt Nutrition Guidelines and the use of lower body mass index cut-off should be considered.

Chylous ascites: total parenteral nutrition as primary therapeutic modality.

A female infant with Down syndrome and congenital chylous ascites presented at birth with respiratory distress secondary to marked abdominal distension. Total parenteral nutrition (TPN) and paracentesis were the primary therapeutic modality. On hyperalimentation, however, ascites initially recurred, requiring additional paracenteses to improve respiratory distress. The chylous ascites, lymphopenia and hypoalbuminemia were relieved after 10 weeks of TPN administration. We recommend a long-term course (10 weeks) of TPN before an exploratory laparatomy and possible surgical intervention are considered.

Effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes.

In vitamin A-deficient children, increased rates of bacterial infections in the intestine have been observed. The adherence of bacteria is a prerequisite for invasion. Thus, the effect of vitamin A deficiency on the adherence of fimbriated and nonfimbriated Salmonella typhimurium to isolated small intestinal enterocytes was studied. Male weanling rats matched by weight were divided into three groups: one group was fed a vitamin A-free diet for 8-12 weeks; another was given the same diet supplemented with retinol acetate; a third group matched for age served as controls. The vitamin A-deficient group showed a significantly lower growth rate and lower serum retinol levels than either the retinol acetate-supplemented or control groups. In all the groups, S. typhimurium possessing mannose-sensitive fimbriae adhered to enterocytes in significantly larger numbers than the nonfimbriated strains. The number of fimbriated S. typhimurium bound to enterocytes from the proximal small intestine was significantly higher in the vitamin A-deficient rats than in the pair-fed vitamin A-supplemented group (19.3 +/- 14.9 versus 7.8 +/- 5.0; p less than 0.05) or the control group (19.3 +/- 14.9 versus 8.7 +/- 3.5, p = 0.01). The specific activities of the enterocytes lactase, sucrase, and maltase and the protein content in the vitamin A-deficient rats were similar to those in the controls. These results demonstrate that vitamin A deficiency in rats is associated with the increased ability of S. typhimurium to adhere to proximal small intestinal enterocytes. However, the possible changes in the membrane of the enterocyte do not include decreases in brush border disaccharidases or protein content.

The impact of development of the gut on infant nutrition.

We have described the developmental pattern of the GI tract, constituent tissues of which do not develop simultaneously, either functionally or morphologically. Dietary modifications to suit the stage of development have been described, and possible changes resulting from these modifications are also discussed. It is important to note that the newborn period is a time in which rapid development is taking place while the GI system is still not fully mature, hence the macro- and micronutrients given during this period should be adjusted both quantitatively and qualitatively to suit the needs of the infant, particularly so if he is premature or compromised.

Computed axial tomographic scanning of the thigh: an alternative method of nutritional assessment in pediatrics.

In this study we compared the findings of computed axial tomographic (CT) scanning of the thigh with the findings of arm anthropometry and urinary creatinine determinations to assess nutrition in children with inflammatory bowel disease receiving total parenteral nutrition. All 14 children received our standard solution for total parenteral nutrition as well as prednisone and sulfasalazine (Azulfidine) therapy. All patients were assessed by arm anthropometry, 24-hour urine collections for creatinine clearance, and CT scanning of the thigh during total parenteral nutrition. Arm muscle and fat area were estimated by anthropometry, and those in the thigh were estimated by CT scanning. Our results show the total muscle area from the CT scan can predict muscle mass calculated from the urinary creatinine excretion rates. In addition, there is a close correlation between the thigh muscle area as measured by CT scanning and the muscle area calculated from urinary creatinine excretion rates. In addition, the comparison of thigh muscle area and thigh fat area to the midarm muscle area and midarm fat area, respectively, showed that the thigh is a better predictor of muscle than fat in the midarm. We conclude that the total thigh muscle area is a better predictor of muscle mass as compared to the midarm muscle area. In addition, the CT scan cut at the level of the thigh in children and adolescents with inflammatory bowel disease can provide valuable information about the thigh compartment and analyses of different cross-sectional areas of the thigh.

Small intestinal mucosal hyperplasia caused by an enterokinase inhibitor from red kidney bean in rats.

A specific enterokinase inhibitor (EKI) was purified from red kidney bean (RKB). Male weanling rats fed a diet containing this purified EKI (0.06%) for 6 d showed increases in mucosal weights, protein, DNA and lactic dehydrogenase contents in their small intestines compared to age-matched control rats fed a standard diet. Total mucosal EK and disaccharidase activities were, however, decreased in EKI-fed rats. Thus, oral consumption of EKI from RKB led to small intestinal mucosal hyperplasia in rats. The mucosal hyperplasia observed in EKI-fed rats is not likely due to decreased turnover of mucosal proteins as a result of reduced luminal proteases since luminal contents of trypsin, chymotrypsin and elastase in EKI-fed rats were similar to those of control rats. Enterokinase inhibitor may have a direct hyperplastic effect on the small intestine of rats.

Carbohydrate digestion: development in early infancy.

Developmental, congenital, and acquired carbohydrate malabsorption syndromes and the particular problems of premature and compromised infants are presented. The clinical features, pathogenesis and intervention strategies for the aforementioned disorders are reviewed.

Pancreatic and intestinal digestive enzymes in post-weanling rats with hypothalamic obesity.

Male Sprague-Dawley rats received bilateral electrolytic lesions in the ventromedial hypothalamic nuclei (VMNL rats) at the age of 31 days; sham-lesioned rats served as controls. For 28 post-operative days all animals self-selected from three synthetic diets, each high in carbohydrate, fat and protein, respectively. Following this, half of the VMNL rats and half of the controls were switched to lab chow for 14 days. Body weights were comparable among the groups, but linear growth was greatly reduced and body fat (Lee Index) was elevated in VMNL rats, irrespective of diet. In the sham-lesioned controls, the synthetic diets reduced most parameters of exocrine pancreatic activity. In VMNL rats, in contrast, pancreatic parameters were unaffected by the synthetic diet. The data suggest that VMN lesions disinhibit the exocrine pancreas. In contrast, most parameters of intestinal activity were not influenced by VMN lesions.

Pancreatic growth and enzyme profiles in weanling rats with normophagic hypothalamic obesity.

Weanling male rats with ventromedial hypothalamic lesions (VMNL rats) and sham-operated controls were killed 1, 2, 4, and 5 weeks postoperatively. The VMNL rats developed normophagic hypothalamic obesity in the presence of normal body weight and reduced linear growth. In both VMNL and control rats, pancreatic weight and protein content increased with time but were lower in the lesioned animals. Pancreatic DNA content was arrested in VMNL rats and remained so during the remainder of the experiment. The only significant enzyme changes (trypsinogen, amylase, and lipase) were evident in higher trypsinogen concentration in VMNL rats during 2 and 4 weeks after lesion production. In view of previous data on both hypophysectomized and VMNL rats and the known role of the ventromedial hypothalamic nucleus in neuroendocrine and neuroautonomic function, it is speculated that the changes observed here are in part due to disruption of neuroendocrine and in part due to disturbance of neuroautonomic control systems.

Effect of glucose and insulin on small intestinal brush border enzymes in fasted rats.

Fasting reduced small intestinal length. It also decreased mucosal weight, DNA and protein content, and concentrations of enterokinase, maltase, and sucrase in both duodenal and jejunal segments. In contrast, the concentrations of lactase and leucine aminopeptidase were not affected. Concomitantly, serum insulin levels dropped to one-fifth of the control levels while serum glucose concentrations showed a lesser degree of reduction. Glucose supplementation alone raised the serum insulin level, prevented the decrease in DNA content, and showed a protective effect on mucosal protein, mucosal weight, mucosal thickness, and villus height. Glucose also protected the sucrase and maltase concentrations; more significantly for maltase in the jejunal segment. Insulin alone, although it increased the serum insulin level to that found with glucose supplementation alone, had no protective effect on the loss in protein, DNA, and most enzymes except for maltase concentration in the jejunal segment. Addition of insulin to glucose did not modify the glucose effect on the contents of DNA, protein, and concentrations of sucrase and maltase. These results suggest that the glucose effect on the mucosa is not mediated by insulin. In addition, the retention of both maltase and sucrase activities through only glucose supplementation suggests the loss of maltase and sucrase in fasting is due to nutrient rather than specific substrate restriction.

Nodular colonic mucosa of childhood: normal or pathologic?

The small colonic mucosal nodules that have been referred to in the past as lymphatic nodular hyperplasia are felt to represent a normal response of the prominent colonic lymphatic tissue in children. To support this hypothesis, a prospective study of all air-contrast barium enemas, colonoscopies, and intestinal biopsies performed during 1 yr was carried out. During that year 48 patients had air-contrast barium enemas, and 21 of these 48 patients also had colonoscopy and mucosal biopsies. Greater than half of the children studied by air-contrast barium enema (26 out of 48) and colonoscopy (12 out of 21) had nodular colonic mucosa. These nodules were described at colonoscopy as being smooth surfaced, yellowish-white, 1-2 mm in diameter. There was no correlation between the presence or absence of these nodules with any symptom or symptom complex. The younger patients, the more frequently these nodules were oberved. No immunologic disorder was associated with the nodular colonic mucosa in the children that were tested. Nodular colonic mucosa in childhood should be considered a frequent finding indicative of normal lymphatic response to nonspecific stimuli, which may often be infectious in nature.

Early detection of adenomatous polyposis coli in Gardner's syndrome.

Gardner's syndrome, an autosomal dominant disorder, consists of multiple polyposis of the colon associated with various soft- and hard-tissue tumors. The appearance of adenomatous hyperplasia and polyposis in at-risk patients before adolescence has not been full appreciated. Four preadolescent children from a kindred with Gardner's syndrome were examined by use of colonoscopy and mucosal biopsy. In three children (18 months, 6 years, and 9 years old) adenomatous hyperplasia or polyposis was found. The colon of the fourth child (3 years old) was normal. The three affected children were asymptomatic. The youngest had a barium enema and results were normal. The oldest child had polyps. Biopsies revealed focal atypical hyperplasia of the glands with pseudostratification of the epithelial cells, frequent mitotic figures, and the absence of goblet cells. More severe manifestations were noted in the splenic flexure than in the sigmoid flexure or rectum. The youngest patient showed early adenomatous hyperplasia characterized by a marked reduction of the goblet cells, especially in the surface epithelium. Colonoscopy and mucosal biopsies are mandatory in at-risk children. By deferring colonic examination until adolescence, a patient is placed at risk for malignant degeneration of the adenomatous tumor.

Recurrent acute pancreatitis in patients with cystic fibrosis with normal pancreatic enzymes.

Ten adolescent and young adults with cystic fibrosis (CF) have had well-documented recurrent attacks of acute pancreatitis. The diagnosis of CF in each patient was delayed because they did not have pancreatic insufficiency. The diagnosis of CF was documented by the typical pulmonary involvement and elevated sweat sodium and chloride levels in all cases and a positive family history in six of the ten patients. Two patients were diagnosed as having acute pancreatitis before the diagnosis of CF was made, thus indicating that acute pancreatitis may be the presenting complaint in the young adult with CF. The diagnosis of acute pancreatitis was based on the presence of severe abdominal pain, usually with vomiting, tenderness in the mid-epigastrium, elevated serum and urinary amylase and serum lipase. Attacks were precipitated by fatty meals, alcohol ingestion; postcholecystectomy and tetracycline administration. In some patients no precipitating event could be elicited. Intravenous secretin-pancreozymin stimulation tests revealed a diminished bicarbonate secretion with little effect on the secretion of the zymogen enzymes. A mild attack of pancreatitis occurred after secretin-pancreozymin stimulation. The endocrine pancreatic function tested in four patients was normal as revealed by the glucose tolerance tests and determinations of serum insulin, growth hormone and free fatty acid. Transduodenal pancreatograms were performed in three patients; one showed a normal pancreatic duct, one showed duct obstruction and in the third patient a beady type of narrowing was found. The selenomethionine Se 75 uptake of the pancreas was noted only in the head of the pancreas. This suggests that loss of function occurs initially to a greater extent in the tail and body of the pancreas. Three patients died and showed characteristic lesions of CF.