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The nutritional health of American Indian and Alaska Native children has changed dramatically over the past 30 years. The prevention and treatment of malnutrition (primarily undernutrition) was a major health issue until the mid to late 1970s. Now, a generation later, obesity in American Indian and Alaska Native children is a major health threat. In 1969, the National Institutes of Health sponsored a conference to review the nutritional status of North American Indian children and to set a national agenda to improve the nutritional health of Indian children. Subsequently, increased food availability; food assistance programs; and improved sanitation, transportation, and health care have eliminated undernutrition as a major health issue. However, the substantial reduction in undernutrition has been accompanied by a rapid increase in childhood obesity. The current epidemic of child and adult obesity and associated obesity-related morbidities, such as type 2 diabetes mellitus and other chronic diseases, has implications for the immediate and long-term health of young American Indians. This article reviews the current nutritional health of American Indian and Alaska Native children, the changes that have occurred the past 30 years, and the nutrition transition to increasing obesity and subsequent diabetes that is being seen in American Indians. Future directions to improve the health of American Indian and Alaska Native children are discussed, as is the urgent need for obesity prevention programs that are culturally oriented, family centered, and community- and school-based and that target healthful eating and physical activity beginning in childhood.
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PMID:Nutritional concerns in American Indian and Alaska Native children: transitions and future directions. 1251 18

A 1991 National Institutes of Health Consensus Conference concluded that severely obese adults could be eligible for bariatric surgery if they had a body mass index (BMI) > or =35 kg/m(2) with or > or =40 kg/m(2) without obesity comorbidity. It was thought at that time that there were inadequate data to support bariatric surgery in severely obese adolescents. An estimated 25% of children in the United States are obese, a number that has doubled over a 30-year period. Very little information has been published on the subject of obesity surgery in adolescents. Therefore we reviewed our 20-year database on bariatric surgery in adolescents. Severely obese adolescents, ranging from 12 to less than 18 years of age, were considered eligible for bariatric surgery according to the National Institutes of Health adult criteria. Gastroplasty was the procedure of choice in the initial 3 years of the study followed by gastric bypass, which was found to be significantly more effective for weight loss in adults. Distal gastric bypass (D-GBP) was used in extremely obese patients (BMI > or =60 kg/m(2)) before 1992 and long-limb gastric bypass (LL-GBP) was used for superobese patients (BMI > or =50 kg/m(2)) after 1992. Laparoscopic gastric bypass was used after 2000. Thirty-three adolescents (27 white, 6 black; 19 females, 14 males) underwent the following bariatric operations between 1981 and June 2001: horizontal gastroplasty in one, vertical banded gastroplasty in two, standard gastric bypass in 17 (2 laparoscopic), LL-GBP in 10, and D-GBP in three. Mean BMI was 52 +/- 11 kg/m(2) (range 38 to 91 kg/m(2)), and mean age was 16 +/- 1 years (range 12.4 to 17.9 years). Preoperative comorbid conditions included the following: type II diabetes mellitus in two patients, hypertension in 11, pseudotumor cerebri in three, gastroesophageal reflux in five, sleep apnea in six, urinary incontinence in two, polycystic ovary syndrome in one, asthma in one, and degenerative joint disease in 11. There were no operative deaths or anastomotic leaks. Early complications included pulmonary embolism in one patient, major wound infection in one, minor wound infections in four, stomal stenoses (endoscopically dilated) in three, and marginal ulcers (medically treated) in four. Late complications included small bowel obstruction in one and incisional hernias in six patients. There were two late sudden deaths (2 years and 6 years postoperatively), but these were unlikely to have been caused by the bariatric surgical procedure. Revision procedures included one D-GBP to gastric bypass for malnutrition and one gastric bypass to LL-GBP for inadequate weight loss. Regain of most or all of the lost weight was seen in five patients at 5 to 10 years after surgery; however, significant weight loss was maintained in the remaining patients for up to 14 years after surgery. Comorbid conditions resolved at 1 year with the exception of hypertension in two patients, gastroesophageal reflux in two, and degenerative joint disease in seven. Self-image was greatly enhanced; eight patients have married and have children, five patients have completed college, and one patient is currently in college. Severe obesity is increasing rapidly in adolescents and is associated with significant comorbidity and social stigmatization. Bariatric surgery in adolescents is safe and is associated with significant weight loss, correction of obesity comorbidity, and improved self-image and socialization. These data strongly support obesity surgery for those unfortunate individuals who may have difficulty obtaining insurance coverage based on the 1991 National Institutes of Health Consensus Conference statement.
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PMID:Bariatric surgery for severely obese adolescents. 1255 91

In persons with diabetes, moderate hyperglycemia can contribute to an increased turnover of protein. To maintain body composition and nitrogen balance requires metabolic control and sufficient protein and energy intakes. However, because most adults eat at least 50% more protein than is required, people with diabetes appear to be protected from protein malnutrition when consuming a usual diet. Although nonessential amino acids undergo hepatic gluconeogenesis, peripheral glucose concentrations do not increase after protein ingestion. The fate of produced glucose is unknown. Protein does not contribute to sustained elevations of glucose levels, slow absorption of carbohydrate, or help in the treatment of hypoglycemia--advice often given to persons with diabetes. Protein is, however, just as potent a stimulant of insulin secretion as glucose. No long-term research is available to document that high-protein, low-carbohydrate diets are continued long-term or that weight lost initially is maintained better from these diets than from traditional weight loss diets. Furthermore, in persons with type 2 diabetes, weight loss is reported to be related to energy restriction and not to the protein-to-carbohydrate ratio of the diet.
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PMID:Protein and diabetes: much advice, little research. 1264 72

Nutritional and genetic factors interact in the etiology of type 2 diabetes. Undernutrition followed by overnutrition increases adiposity and the risk of diabetes. The thrifty hypotheses suggest that the nutritional challenges could have happened thousands of year ago (thrifty gene selection) or during one's intrauterine life (thrifty phenotype). Current strategies for the prevention of diabetes are related to avoiding overnutrition.
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PMID:Nutrition, growth, and body size in relation to insulin resistance and type 2 diabetes. 1272 36

Based on our investigations in first-degree relatives, in twins in general, and in monozygotic twins discordant for type 2 diabetes, we have studied the inheritance of glucose intolerance, insulin resistance and insulin secretion in order to evaluate the role of genes versus environment in the development of type 2 diabetes. Insulin resistance in type 2 diabetes is mainly linked to glucose disposal in skeletal muscle, i.e. reduced glycogen synthesis. In order to investigate the genetic component responsible for the reduced glycogen synthase activity and reduced glucose transport, we also investigated cultured myotubes based on in vivo skeletal muscle biopsies. The results obtained in our own studies are discussed in comparison with the international literature. We conclude that both genetic and environmental factors play a role in the development of type 2 diabetes (hyperglycaemia), and that only subjects who are genetically disposed to insulin resistance and who possess beta-cells which are unable to compensate for the degree of insulin resistance seem to develop type 2 diabetes. Variables of two gene alleles disposing to insulin resistance have been identified, and their role is discussed. The most important environmental factor seems to be obesity, but intrauterine malnutrition also plays a role. The cellular mechanism responsible for obesity/lipid-induced diabetes mellitus is discussed with specific emphasis on the role of accumulation of long-chain AcylCoA and triglycerides in liver, muscle and beta-cells.
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PMID:Metabolic and genetic influence on glucose metabolism in type 2 diabetic subjects--experiences from relatives and twin studies. 1296 96

Insulin receptor substrate-2(IRS-2) belongs to a family of cytoplasmic adaptor proteins, which link insulin, insulin-like growth factor-1(IGF-1), and cytokine receptor tyrosine kinases to signaling pathways regulating metabolism, growth, differentiation, reproduction, and homestasis. Deficiency of IRS-2 in mice causes type 2 diabetes mellitus (T2DM), suggesting that abnormal structure and dysfunction of the IRS-2 gene may contribute to the pathogenesis of T2DM. Variations in the open reading frame (ORF) and promoter region of IRS-2 gene in patients with T2DM have been reported over the past few years. These genetic variations are from ethnically different patients, confounding any analysis of the contribution of IRS-2 gene variations to the development of T2DM. The 3'-untranslated region(3'-UTR) of IRS-2 gene variation may be contribute to the T2DM. So far, the relationship between 3'-UTR of IRS-2 gene variations and T2DM have not been investigated. Based on the 3'-UTR of eukaryotic gene plays an important role in the eukaryotic gene regulation, we investigated abnormalities of IRS-2 gene 3'-UTR and their relation with T2DM in the Chinese population. Genomic DNA was extracted from leukocyte of 128 patients with T2DM and 125 control subjects in Hunan, China. A segment of IRS-2 gene 3'-UTR was scanned by polymerase chain reaction (PCR)-denaturing high-performance liquid chromatography (DHPLC). All PCR products with abnormal DHPLC pattern were submitted to DNA sequence analysis. A T-->C mutation at 4064 bp of IRS-2 gene 3'-UTR was found in 18 patients with T2DM, while it was only found in 5 control subjects. The incidence of the mutation in patients with T2DM were much higher than that in contol subjects (14.1% vs 4.0%, x2 = 7.748, P = 0.005). These results indicate that the T4064-->C in IRS-2 gene 3'-UTR may be related to Chinese patients with T2DM.
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PMID:[Variation of insulin receptor substrate-2 gene 3'-untranslated region in patients with type 2 diabetes mellitus]. 1468 50

Nutritional deprivation of the fetus and infant is associated with susceptibility to the development of impaired glucose tolerance or type 2 diabetes in adult life. Quantitative changes in mitochondrial DNA (mtDNA) seem to be associated with type 2 diabetes, but the effect of protein malnutrition on mtDNA content is not known. This study investigated the effects of protein malnutrition in fetus and early life on mtDNA content and glucose-insulin metabolism in adult life. Male offspring of dams fed a low-protein (LP) diet (8% casein) during pregnancy and lactation were weaned onto either a control (18% casein) diet (recuperated group, R) or a LP diet, and they were compared with the control group (C). The mtDNA content in the liver was lower in the R and LP groups than in the C group at 5 weeks of age, but higher in the R and LP groups than in the C group at 15 weeks of age. The mtDNA content in skeletal muscle and pancreas was significantly lower in the R and LP groups than in the C group at 25 weeks of age. Fetal-malnourished rats showed decreased pancreatic beta-cell mass and reduced insulin secretory responses to glucose load, but no differences in glucose tolerance or insulin sensitivity. Our findings imply that protein malnutrition in utero causes changes in mtDNA content, impaired beta-cell development, and insulin secretion, which may contribute to the development of type 2 diabetes in later life.
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PMID:Changes of mitochondrial DNA content in the male offspring of protein-malnourished rats. 1512 98

The metabolic syndrome (MetS) is a huge public health problem worldwide, being one of the major causes of cardiovascular disease, responsible for a growing number of premature deaths throughout the world. MetS includes a cluster of anomalies, such as: abdominal obesity, insulin resistance, hyperinsulinemia, hypertension, type 2 diabetes mellitus or glucose intolerance, hypertriglyceridemia etc. The number of people with MetS increases with age, affecting more than 40% of people in their 60s and 70s. About 30% of European people over 50 have MetS. Some experts estimate that as many as two thirds of Americans may be suffering from MetS. The exact cause of MetS is not known: genetics play a minor role, acquired in-utero factors also play a role (prenatal malnutrition, toxin exposure, exposure to high levels of maternal cortisol). For most people, the MetS results primarily from lifestyle factors, such as: chronic stress, inadequate exercise. The MetS can be avoided and reversed in most cases. Weight loss is both a treatment and goal for MetS patients. Moderate weight loss, in the range of 5-10% of body weight, can help restore body's ability to recognize insulin and greatly reduce the chance that the syndrome will evolve into a more serious illness. In most people weight loss will lower blood pressure and improve triglyceride levels. Increased activity alone can improve insulin levels. Physical activity result in a weight loss, improved blood pressure, improved cholesterol and triglyceride level and reduced risk of developing diabetes. It is also important to treat: hyperlipidemia, hypertension, prothrombotic state.
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PMID:The metabolic syndrome--a multifaced disease. 1552 15

Metabolism cycles daily between the fed and fasted states. The pathways of energy production are reversible and distinct. In the anabolic (fed) state, the liver stores glucose as glycogen, and fatty acid/triglyceride synthesis is active. In the catabolic (fasted) state, the liver becomes a glucose producer, lipogenesis is slowed, and fatty acid oxidation/ketogenesis is activated. The rate-limiting step for the latter is vested in the carnitine/carnitine palmitoyltransferase (CPT) system, and the off/on regulator of this is malonyl CoA. The AMP-induced protein kinase primarily determines the concentration of malonyl CoA. Four other systems have significant influence: two on fatty acid oxidation and two on lipogenesis. Peroxisome proliferator-activated receptor gamma-1 alpha, a master regulator of metabolism, induces hepatic gluconeogenesis and fatty acid oxidation in the catabolic phase. Deficiency of stearoyl CoA desaturase, although having no role in gluconeogenesis, powerfully induces fatty acid oxidation and weight loss despite increased food intake in rodents. Major stimulators of lipogenesis are carbohydrate-responsive element binding protein and the Insig system. The malonyl CoA-regulated CPT system has been firmly established in humans. The other systems have not yet been confirmed in humans, but likely are active there as well. Activation of fatty acid oxidation has considerable clinical promise for the treatment of obesity, type 2 diabetes, steatohepatitis, and lipotoxic damage to the heart.
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PMID:The role of the carnitine system in human metabolism. 1559 Sep 99

Although pancreatic beta-cells are capable of adapting their mass in response to insulin requirements, evidence has shown that a dietary insult could compromise this ability. Fetal malnutrition has been linked to low birth weight and the development of type 2 diabetes later in life, while reduced beta-cell mass has been reported in adult rats fed a high-fat diet (HFD). Reported here are the effects of exposure to a HFD, during different periods of gestation, on neonatal rat weight and beta- and alpha-cell development. The experimental groups were composed of neonatal offspring obtained from Wistar rats fed a high-fat (40% as energy) diet for either the first (HF1), second (HF2), or third (HF3) week, or all three (HF1-3) weeks of gestation. Neonatal weights and circulating glucose and insulin concentrations were measured on postnatal day 1, after which the pancreata were excised and processed for histological immunocytochemical examination and image analysis. HF1 and HF2 neonates were hypoglycemic, whereas HF1-3 neonates were hyperglycemic. Low birth weights were observed only in HF1 neonates. No significant differences were detected in the circulating insulin concentrations in the neonates, although beta-cell volume and numbers were reduced in HF1-3 neonates. beta-cell numbers also declined in HF1 and HF3 neonates. alpha-cell volume, number and size were, however, increased in HF1-3 neonates. alpha-cell size was also increased in HF1 and HF3 neonates. In neonates, exposure to a maternal HFD throughout gestation was found to have the most adverse effect on beta-cell development and resulted in hyperglycemia.
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PMID:Islet cell response in the neonatal rat after exposure to a high-fat diet during pregnancy. 1570 4


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