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Query: UMLS:C0028754 (
obesity
)
124,988
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Anastomotic leakage is a major cause of mortality in colorectal surgery. Some variables associated with a high-risk level for anastomotic leakage have been identified, including denutrition,
obesity
, smoking, level of the anastomoses, qualification of the surgeon. Several methods have been evaluated in order to prevent anastomotic leakage. Prophylactic antibiotic therapy has been recommended, but has no effect on the rate of anastomotic leakage. Optimal preoperative colonic preparation appears to be obtained with povidone
iodine
enemas associated with a low residue diet. Stapling gives better results than sutures only for difficult anastomoses. Colostomy does not prevent leakage but minimizes its consequences. Omentoplasty, peritoneal drainage, gastric tube, biofragmentable anastomotic ring, and Coloshield have demonstrated their efficacy.
...
PMID:[Prevention of anastomotic dehiscence in colorectal surgery]. 1079 Jun 19
The aim of this retrospective study was to investigate the frequency of thyroid dysfunction as assessed by TSH, T3 and T4 in a large cohort of 290 obese and 280 healthy children. In addition, thyroid autoantibodies were measured in random subgroups of 123 obese and 80 control children,
iodine
excretion in 50 and thyroid volume in 23 of the obese children. Elevated TSH levels (>4 U/l) were found in 22 obese children (7.5%), but only in one control (0.3%). The medians of TSH and T3 concentrations were normal, but significantly higher in the obese group than in the controls, while T4 levels did not differ. The prevalence of positive thyroid autoantibodies was increased in the obese children, for the most part in those with elevated TSH. There was no evidence for
iodine
deficiency as a cause of the average increase of TSH. We conclude that in childhood
obesity
TSH and T3 levels are significantly increased; in most cases, however, these increases are not accounted for by thyroid autoimmunity or
iodine
deficiency. As a consequence, TSH elevations with normal thyroid hormone levels in obese children don't need any thyroxine treatment, if thyroid disorders were definitely excluded beforehand.
...
PMID:Thyroid function and obesity in children and adolescents. 1118 30
Thyroid function tests might be affected by diabetes and
obesity
. To evaluate the influence of these parameters in routine conditions, 72 diabetic and 53 non-diabetic outpatients without known thyroid diseases or severe chronic illness were recruited over a 7-month period. For each patient, dosages of thyrotropin (TSH), total and free thyroxine (TT4 and FT4, respectively), total and free triiodothyronine (TT3 and FT3) and T3 resin uptake (T3RU) were performed by radioimmunoassays. The simultaneous influence of various parameters known to affect thyroid-function tests was evaluated by multivariate linear regression. The studied variables included gender, age, glucosteroids, estrogens, tobacco habits,
iodine
contacts, body mass index (BMI) and diabetes mellitus. Tobacco habits and
iodine
contacts did not influence any tests. As expected, estrogens induced an increase in TT4 and TT3 values (p < 0.001 and 0.020, respectively) associated with a decrease in T3RU (p < 0.001). Consequently, females had lower T3RU than males (p < 0.0001). Corticotherapy was associated with decreased TSH values (p = 0.022). TT3 and FT3 decreased with age (p < 0.001), whereas T3RU and FT4 increased (p = 0.020 and 0.004, respectively). In contrast to an increase in TSH (p = 0.006), TT4 and FT4 decreased at higher BMI levels (p = 0.018 and 0.004, respectively), which is consistent with subclinical hypothyroidism. In diabetic patients, TSH was lower than in nondiabetic subjects (p = 0.039). Thus, the present study indicates that besides known parameters such as age and drugs, thyroid-function tests can also be altered by diabetes mellitus and
obesity
.
...
PMID:Minor alterations in thyroid-function tests associated with diabetes mellitus and obesity in outpatients without known thyroid illness. 1138 17
Obesity
is associated with insulin resistance and some reproductive abnormalities. Circulating FFAs are often elevated in obese subjects and are also closely linked to insulin resistance. In this study, we demonstrated that saturated FFAs, such as palmitic acid and stearic acid, markedly suppressed the granulosa cell survival in a time- and dose-dependent manner. Polyunsaturated FFA, arachidonic acid, had no effect on the cell survival, even at supraphysiological concentrations. The suppressive effect of saturated FFAs on cell survival was caused by apoptosis, as evidenced by DNA ladder formation and annexin V-EGFP/propidium
iodide
staining of the cells. The apoptotic effects of palmitic acid and stearic acid were unrelated to the increase of ceramide generation or nitric oxide production and were also completely blocked by Triacsin C, an inhibitor of acylcoenzyme A synthetase. In addition, acylcoenzyme A, pamitoylcoenzyme A, and stearylcoenzyme A markedly suppressed granulosa cell survival, whereas arachidonoylcoenzyme A had no such effect, and this finding was consistent with the effect of the respective FFA form. Surprisingly, arachidonic acid instead showed a protective effect on palmitic acid- and stearic acid-induced cell apoptosis. A Western blot analysis showed the apoptosis of the granulosa cells induced by palmitic acid to be accompanied by the down-regulation of an apoptosis inhibitor, Bcl-2, and the up-regulation of an apoptosis effector, Bax. These results indicate that saturated FFAs induce apoptosis in human granulosa cells caused by the metabolism of the respective acylcoenzyme A form, and the actual composition of circulating FFAs may thus play a critical role in the apoptotic events of human granulosa cells. These effects of FFAs on granulosa cell survival may be a possible mechanism for reproductive abnormalities, such as amenorrhea, which is frequently observed in obese women.
...
PMID:Saturated FFAs, palmitic acid and stearic acid, induce apoptosis in human granulosa cells. 1145 7
We analyzed the genetic regulation of spontaneous autoimmune thyroiditis (SAT) by means of crosses between
Obese
strain (OS) chickens with the disease, and healthy inbred chicken of line CB. Mononuclear cell infiltration of the thyroid was used as a criterion for the disease. We confirmed the existence of one recessive gene, regulating the susceptibility of the thyroid gland to autoimmune attack. From the frequency of progeny with the thyroid infiltration in backcross and F2 generations, we presume the existence of one or two additional dominant genes coding for abnormal reactivity of the immune system. The total number of genes regulating SAT is therefore a maximum of three. We attempted to identify disease-specific transcripts responsible for the initiation of the disease using suppression subtractive hybridization of RNA prepared from OS and CB thyroid lobes, obtained from 3-day-old chicks. From forward and reverse subtractions, we recovered a fragment mixture in the range of 300 bp to 1.5 kb. In total, 768 clones were screened and 9 were sequenced. Four of them represent unknown sequences. Two, specific for OS thyroid, correspond to envelope genes of avian endogenous viruses (ev)-1, -3 and -6. The expressed product of an env gene could be iodinated in the thyroid gland and become involved in thyroglobulin metabolism. This may be another possible mechanism driving SAT, as
iodine
modulates SAT in the chicken. Further experiments will be required to prove this hypothesis. Two thyroid-specific clones had significant alignment to human thyroglobulin, and one clone to human coatomer protein. We analyzed, by RFLP and RNA dot blots, cosegregation between clones for the env gene of endogenous viruses as the most promising candidate for involvement in driving SAT; we did not find differences at the DNA and RNA levels. We can possibly therefore rule out a simple involvement of env genes with the initiation of disease.
...
PMID:Analysis of genetic regulation of chicken spontaneous autoimmune thyroiditis, an animal model of human Hashimoto's thyroiditis. 1186 10
Achievement of Health-for-All, whereby people everywhere throughout their lives, have the opportunity to reach and maintain the highest attainable level of health is impossible whilst hunger, starvation, and malnutrition remain. Malnutrition covers a broad spectrum of ills, including undernutrition, specific nutrient deficiencies, and overnutrition; and it kills, maims, retards, cripples, blinds, and impairs human development on a truly massive scale worldwide. In the developing world in 1995, of the estimated 10.4 million deaths among children under 5 years of age, protein-energy malnutrition was an associated and causative factor in 5.1 million of these deaths (i.e. 49%). On the other hand, evidence has recently been compiled suggesting that of the more than 10 million cases of cancer that occurred in 1996, an estimated 30-40% (3-4 million every year) are preventable by feasible, appropriate diets, and by physical activity and maintenance of appropriate body weight. Malnutrition affects all age groups across the entire lifespan. From the moment of conception, throughout foetal life,
iodine
, folate and intrauterine nutrition have a profound influence on development, growth, morbidity, mortality, not only in utero and in early infancy, but on morbidity, physical and mental capacity throughout life. Despite significant improvements in world food supplies, health conditions, and availability of educational and social services, no population escapes malnutrition's grasp. All countries have significant population groups with some form of debilitating malnutrition. Malnutrition worldwide, includes a spectrum of nutrient-related disorders, deficiencies and conditions including the following major public health problems; Intrauterine growth retardation, protein-energy malnutrition, Iodine deficiency disorders, Vitamin A Deficiency, Iron Deficiency Anaemia and Overweight and
Obesity
(WHO, Website).
...
PMID:The emerging importance of dietary lipids, quantity and quality, in the global disease burden: the potential of aquatic resources. 1200 80
The author contends that neither behavioral nor psychological factors are responsible for
obesity
or overweight, but that physiological and nutritional factors are.
Obesity
and overweight are relevant to natural family planning because they contribute to various problems of the female reproductive system. Body fat stores estrogen, and excess body fat increases estrogen levels which creates various problems. For example, elevated estrogen levels may contribute to endometrium build-up, resulting in heavy, prolonged bleeding during menstruation or in midcycle. They may kick off a reaction, causing suppressed ovulation, premenstrual spotting, and menstrual cramps. Other possible effects of high estrogen levels are fibroid tumors, breast cancer, endometrial cancer, ovarian cancer, and amenorrhea. The consistent pressure of excess body fat on the uterus can result in uterine prolapse. Overweight may also be a symptom of a reproductive problem, e.g., ovarian failure. Hypoglycemia, including reactive hypoglycemia, caused by a diet high in sugar and white flour, plays a key role in overweight. Excessive insulin secretion in reactive hypoglycemic cases maintains high glucose levels, and the body stores the excess glucose in fat cells. Thus, a diet low in sugary foods and high in fiber-rich complex carbohydrates is the most successful way to lose weight. However, vitamins and minerals needed to maintain blood sugar levels must supplement this diet to be successful. These vitamins and minerals include the B vitamins, magnesium, and, perhaps, chromium.
Iodine
, vitamins A and E, zinc, and selenium help the thyroid gland operate optimally, so as to avoid excess blood sugar levels. Vitamin E, lecithin, and evening primrose oil assist the body in using fat better. Regular exercise is also important to burn excess fat. Aspartame (Nutrasweet) exacerbates hypoglycemia and is usually found in refined foods and non-foods.
...
PMID:An empathetic look at overweight. 1231 98
A few months ago, the Brazilian Society for Neuroscience and Behavior (SBNeC) promoted a "virtual symposium" (by Internet, under the coordination of R.C.A. Guedes) on "Nutrition and Brain Function". The discussions generated during that symposium originated the present text, which analyzes current topics on the theme, based on the multidisciplinary experience of the authors. The way the brain could be non-homogeneously affected by nutritional alterations, as well as questions like early malnutrition and the development of late
obesity
and hormone abnormalities were discussed. Also, topics like the role of essential fatty acids (EFAs) on brain development, increased seizure susceptibility and changes in different neurotransmitters and in cognitive performance in malnourished animals, as well as differences between overall changes in nutrient intake and excess or deficiency of specific nutrients (e.g.
iodine
deficiency) were analyzed. It was pointed out that different types of neurons, possibly in distinct brain structures, might be differently affected by nutritional manipulation, including not only lack-but also excess of nutrient intake. Such differences could help in explaining discrepancies between data on humans and in animals and so, could aid in determining the basic mechanisms underlying lesions or changes in brain function and behavior.
...
PMID:Nutrition and brain function: a multidisciplinary virtual symposium. 1238 93
In men,
obesity
has generally been associated with reduced plasma testosterone levels and with elevation of the plasma free fatty acids (FFAs). In this study, we investigated the effects of saturated FFAs including palmitic acid (PA) and stearic acid (SA), and polyunsaturated FFA arachidonic acid (AA) on the survival of rat testicular Leydig cell cultured in vitro. PA and SA markedly suppressed Leydig cell survival in a time- and dose-dependent manner. In contrast, AA stimulated the cell proliferation at 5-10 times of physiological concentration. The suppressive effect of PA and SA on cell survival was caused by apoptosis evidenced by DNA ladder formation and Annexin V-EGFP/propidium
iodide
staining of the cells. The apoptotic effect of PA was possibly mediated by ceramide generation because it could be completely blocked by ceramide synthase inhibitor fumonisin B1 and exogenous ceramide itself could directly induce apoptosis in vitro. Surprisingly, the apoptosis induced by PA could be partly prevented by AA. These results indicate that PA and SA induce apoptosis in testicular Leydig cells by ceramide production and these apoptotic effects may be a possible mechanism for reproductive abnormalities in obese men, and AA can partly prevent the apoptotic effect induced by saturated FFA.
...
PMID:Saturated free fatty acids, palmitic acid and stearic acid, induce apoptosis by stimulation of ceramide generation in rat testicular Leydig cell. 1268 33
Uncouplers of oxidative phosphorylation have relevance to bioenergetics and
obesity
. The mechanisms of action of chemical uncouplers of oxidative phosphorylation on biological systems were evaluated using differential gene expression. The transcriptional response in human rhabdomyosarcoma cell line (RD), was elucidated following treatment with carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP), a classical uncoupling agent. Changes in mitochondrial membrane potential were used as the biological dosimeter. There was an increase in membrane depolarization with increasing concentrations of FCCP. The concentration at 75% uncoupling (20 microM) was chosen to study gene expression changes, using cDNA-based large-scale differential gene expression (LSDGE) platforms. At the above concentration, subtle light microscopic and clear gene expression changes were observed at 1, 2, and 10 h. Statistically significant transcriptional changes were largely associated with protein synthesis, cell cycle regulation, cytoskeletal proteins, energy metabolism, apoptosis, and inflammatory mediators. Bromodeoxyuridine (BrdU) and propidium
iodide
(PI) assays revealed cell cycle arrest to occur in the G1 and S phases. There was a significant initial decrease in the intracellular adenosine triphosphate (ATP) concentrations. The following seven genes were selected as potential molecular markers for chemical uncouplers: seryl-tRNA synthetase (Ser-tRS), glutamine-hydrolyzing asparagine synthetase (Glut-HAS), mitochondrial bifunctional methylenetetrahydrofolate dehydrogenase (Mit BMD), mitochondrial heat shock 10-kDa protein (Mit HSP 10), proliferating cyclic nuclear antigen (PCNA), cytoplasmic beta-actin (Act B), and growth arrest and DNA damage-inducible protein 153 (GADD153). Transcriptional changes of all seven genes were later confirmed with reverse transcription-polymerase chain reaction (RT-PCR). These results suggest that gene expression changes may provide a sensitive indicator of uncoupling in response to chemical exposure.
...
PMID:Effects of minimally toxic levels of carbonyl cyanide P-(trifluoromethoxy) phenylhydrazone (FCCP), elucidated through differential gene expression with biochemical and morphological correlations. 1270 Apr
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