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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the work was to investigate: Whether osteoarthritis of the hip can be divided into radiologic classes by examining the tendency of osteoarthritis of the hips to increase the growth and calcific content of the bone on the one hand and the associated loss of calcium and cartilage and the deformation and destruction of bone on the other. The prevalence of osteoarthritis of the hip in the internal medicinal and surgical outpatients of the University Central Hospital of Oulu, who were radiographed. Whether osteoarthritis of the hip or its different radiologic manifestations correlate with the patient's age, sex, occupation and strenuousity of work, rickets, cancerous diseases, diabetes, rheumatoid arthritis, family history, parity, smoking, obesity, physical activity, corticosteroid and anti-epileptic medication, and previous injuries to the lower extremities causing immobilization. Whether the radiologic findings of osteoarthritis of the hip are associated with typical symptoms. Whether there are correlations between the effects of medication and physiotherapy and the radiologic forms of osteoarthritis of the hip. The study population consisted of two series, of which the first included 401 patients: 167 males and 234 females. The second, or major part comprised 518 patients, of whom 249 were male and 269 female. For all these patients we had radiograms available which permitted reliable assessment of the hip condition. The second series, i.e. the latter group of 518 patients, also filled in a questionnaire which dealt with the etiology and symptoms of the osteoarthritis of the hip as well as the therapies they had received. Whenever possible, the changes of the pelvis and the lumbar spine were also assessed on the basis of the radiograms. On the basis of the radiologic findings, osteoarthritis of the hip was divided into two qualitative classes, hypertrophic and destructive, and a mixed type, and into three grades of severity. Hypertrophic osteoarthritis of the hips accounted for 51% of the cases, destructive for 20% and mixed type for 29%. The percentages for the different severities were 47% for the mild, 16% for the moderately severe and 37% for the severe. A total of 26% of the cases were right-sided, 22% left-sided and 52% bilateral. The mild, bilateral cases of osteoarthritis were mostly hypertrophic, whereas destructive osteoarthritis was clearly more common in the unilateral cases. Hypertrophic osteoarthritis was also more frequent in younger age-groups and destructive in older age-groups. The osteoarthritis of the older patients was more severe.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Osteoarthritis of the hip. Radiologic findings and etiology. 391 67

Obesity is characterized by adipocyte hypertrophy and macrophage accumulation in adipose tissue. Monocyte chemoattractant protein-1 (MCP-1) plays a role in macrophage recruitment into adipose tissue. However, other adipocyte-derived factors, e.g., hyaluronan and serum amyloid A (SAA), can facilitate monocyte adhesion and chemotaxis, respectively. The objective was to test the potential involvement of these factors in macrophage recruitment. Differentiated 3T3-L1 adipocytes made hypertrophic by growth in high glucose conditions were used to study SAA and hyaluronan regulation in vitro. Two mouse models of obesity were used to study their expression in vivo. Nuclear factor-kappaB was upregulated and peroxisome proliferator-activated receptor (PPAR)gamma was downregulated in hypertrophic 3T3-L1 cells, with increased expression of SAA3 and increased hyaluronan production. Rosiglitazone, a PPARgamma agonist, reversed these changes. Hypertrophic adipocytes demonstrated overexpression of SAA3 and hyaluronan synthase 2 in vitro and in vivo in diet-induced and genetic obesity. SAA and hyaluronan existed as part of a complex matrix that increased the adhesion and retention of monocytes. This complex, purified by binding to a biotinylated hyaluronan binding protein affinity column, also showed monocyte chemotactic activity, which was dependent on the presence of SAA3 and hyaluronan but independent of MCP-1. We hypothesize that adipocyte hypertrophy leads to increased production of SAA and hyaluronan, which act in concert to recruit and retain monocytes, thereby leading to local inflammation in adipose tissue.
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PMID:Adipocyte-derived serum amyloid A3 and hyaluronan play a role in monocyte recruitment and adhesion. 1756 62

In perinatal medicine, severe obesity of the mother occurs in approximately 1% of cases. This is a problem of increasing importance because of the rising prevalence of juvenile obesity. Our retrospective cohort study aimed at characterising high-risk pregnancies associated with morbid obesity (body mass index [BMI]> or =40). This is of interest not only from an epidemiological perspective and for developing guidelines for clinical care but also from an anthropological point of view. We analysed the German perinatal statistics of the years 1998-2000 with data from more than 500,000 pregnancies. Pregnant women with coexistent morbid obesity were compared to a normal weight reference sample with regard to gestational, perinatal and neonatal risks. Birth weight percentiles were used to classify the neonates according to size (hypotrophy if <10th, hypertrophy/foetal macrosomia if >90th). The obtained risk profile for morbidly obese pregnant women primarily showed pregnancy related diseases, such as hypertension, pre-eclampsia and gestational diabetes. Hypertension and signs of foetal hypoxaemia occurred at higher frequencies with morbid obesity. Hypertrophic neonates were born 3.3 times more often to obese mothers than to mothers of the normal weight. At a BMI> or =40 the rates of complications such as pre-eclampsia, gestational diabetes, impending foetal hypoxaemia, foetal macrosomia, as well as neonatal infections and hyperbilirubinaemia were significantly higher. Obesity and maternal comorbidities, accounted for a higher rate of caesarean sections of up to 38.4% at a BMI> or =45. All differences were highly significant. Preconceptionally, the therapeutic approach should be weight reduction.
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PMID:Morbid obesity: pregnancy risks, birth risks and status of the newborn. 2004 87

The Spontaneously Diabetic Torii (SDT) fatty rat, established by introducing the fa allele of the Zucker fatty rat into the SDT rat genome, is a new model of obesity/type 2 diabetes. The present study investigated effects of food restriction on metabolic and endocrinological function in SDT fatty rats. SDT fatty rats were pair-fed with SDT rats from 7 to 21 weeks of age. The SDT fatty rats were already hyperinsulinemic and hyperlipidemic at 7 weeks of age. After 7 weeks of age, SDT fatty rats showed age-dependently increasing serum glucose levels associated with decreasing serum insulin levels. However, in pair-fed SDT fatty rats, hyperglycemia and hyperinsulinemia were attenuated at 9 weeks of age. After 9 weeks of age, the serum insulin levels unexpectedly increased in the pair-fed SDT fatty rats. Glucose tolerance was also improved, and the pancreatic insulin contents were increased in these rats. Pancreatic islets were hypertrophied in pair-fed SDT fatty rats compared with ad lib-fed SDT fatty rats, which were comparable to SDT rats. This study showed that, in SDT fatty rats, calorie restriction by paired-feeding with SDT rats attenuated hyperglycemia and hyperinsulinemia for the first 2 weeks. Thereafter, the serum insulin levels and pancreatic insulin contents were increased, though the restriction was continued. Hypertrophic pancreatic islets were also remarkable, indicating increased beta cell proliferation. The activated pancreatic beta cell functions might be due to rapid food ingestion, a change of feeding behavior resulting form increasing the fasting period, which was indispensable for calorie restriction.
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PMID:Effects of food restriction on pancreatic islets in Spontaneously Diabetic Torii fatty rats. 2087 55

A combined medico-surgical treatment of obesity illustrates the possibility of achieving harmony of body contours with minimal scarring, risks to the patient, and effort on his or her part. Daily injections of 125 IU of human chorionic gonadotrophin, combined with a special 500-calorie diet, has proven to be a successful medical treatment in more than 6,000 patients treated over a period of 12 years. It had a rapid effect in reducing body contour circumferences over the full course of treatment, and offered the patient a sense of well-being and satisfaction. Mildly overweight responded to this treatment without surgery, a "knifeless torsoplasty." High-risk obese patients were prepared for subsequent surgery. Hypertrophic deformities in a single body area were corrected into a well-proportioned silhouette.
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PMID:Combined medico-surgical torsoplasty. 2417 74

Polycystic ovary syndrome (PCOS), a complex condition that affects women of reproductive age, is characterized by ovulatory dysfunction and androgen excess. Women with PCOS present higher prevalence of obesity, central adiposity, and dyslipidemia, and face increased risk of type 2 diabetes. PCOS is closely linked to functional derangements in adipose tissue. Adipocytes seem to be prone to hypertrophy when exposed to androgen excess, as experienced by women with PCOS, and both adipose tissue hypertrophy and hyperandrogenism are related to insulin resistance. Hypertrophic adipocytes are more susceptible to inflammation, apoptosis, fibrosis, and release of free fatty acids. Disturbed secretion of adipokines may also impact the pathophysiology of PCOS through their influence on metabolism and on sex steroid secretion. Chronic low-grade inflammation in PCOS is also related to hyperandrogenism and to the hypertrophy of adipocytes, causing compression phenomena in the stromal vessels, leading to adipose tissue hypoperfusion and altered secretion of cytokines. Lifestyle changes are the first-line intervention for reducing metabolic risks in PCOS and the addition of an insulin-sensitizing drug might be required. Nevertheless, there is not sufficient evidence in favor of any specific pharmacologic therapies to directly oppose inflammation. Further studies are warranted to identify an adipokine that could serve as an indirect marker of adipocyte production in PCOS, representing a reliable sign of metabolic alteration in this syndrome.
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PMID:Adipose tissue dysfunction, adipokines, and low-grade chronic inflammation in polycystic ovary syndrome. 2562 42

Cardiomyocyte (CM) hypertrophy and increased heart mass in response to pressure overload are associated with hyper-activation of the myocyte enhancer factor-2 (MEF2) family of transcriptional regulators, and concomitant initiation of the fetal gene program. Adiponectin, an adipokine that is reduced in individuals with obesity and diabetes, has been characterized both as a negative regulator or permissive factor in cardiac hypertrophy. We therefore sought to analyze temporal regulation of MEF2 activity in response to pressure overload (PO) and changes in adiponectin status. To address this we crossed a well characterized transgenic MEF2 "sensor" mouse (MEF2-lacZ) with adiponectin null mice (Ad-KO) to create compound MEF2 lacZ/Ad-KO mice. Initially, we established that transverse aortic banding induced PO in wild-type (WT) mice increased heart mass and CM hypertrophy from 1 to 4weeks following surgery, indicated by increased CM diameter and heart weight/tibia length ratio. This was associated with cardiac dysfunction determined by echocardiography. Hypertrophic changes and dysfunction were observed in Ad-KO mice 4weeks following surgery. MEF2 lacZ activity and endogenous ANF mRNA levels, used as indicators of hypertrophic gene activation, were both robustly increased in WT mice after MTAB but attenuated in the Ad-KO background. Furthermore, activation of the pro-hypertrophic molecule p38 was increased following MTAB surgery in WT mice, but not in Ad-KO animals, and treatment of primary isolated CM with recombinant adiponectin induced p38 phosphorylation in a time dependent manner. Adiponectin also increased MEF2 activation in primary cardiomyocytes, an effect attenuated by p38 MAPK inhibition. In conclusion, our data indicate that robust hypertrophic MEF2 activation in the heart in vivo requires a background of adiponectin signaling and that adiponectin signaling in primary isolated CM directly enhances MEF2 activity through activation of p38 MAPK. We conclude that adiponectin is required for full induction of cardiomyocyte MEF2 activation, thus contributing to the myocardial hypertrophic gene expression program in response to PO.
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PMID:Adiponectin is required for cardiac MEF2 activation during pressure overload induced hypertrophy. 2619 5

Obesity is characterized by the chronic low-grade activation of the innate immune system. In this respect, macrophage-elicited metabolic inflammation and adipocyte-macrophage interaction has a primary importance in obesity. Large amounts of macrophages are accumulated by different mechanisms in obese adipose tissue. Hypertrophic adipocyte-derived chemotactic monocyte chemoattractant protein-1 (MCP-1)/C-C chemokine receptor 2 (CCR2) pathway also promotes more macrophage accumulation into the obese adipose tissue. However, increased local extracellular lipid concentrations is a final mechanism for adipose tissue macrophage accumulation. A paracrine loop involving free fatty acids and tumor necrosis factor-alpha (TNF-alpha) between adipocytes and macrophages establishes a vicious cycle that aggravates inflammatory changes in the adipose tissue. Adipocyte-specific caspase-1 and production of interleukin-1beta (IL-1beta) by macrophages; both adipocyte and macrophage induction by toll like receptor-4 (TLR4) through nuclear factor-kappaB (NF-kappaB) activation; free fatty acid-induced and TLR-mediated activation of c-Jun N-terminal kinase (JNK)-related pro-inflammatory pathways in CD11c+ immune cells; are effective in macrophage accumulation and in the development of adipose tissue inflammation. Old adipocytes are removed by macrophages through trogocytosis or sending an "eat me" signal. The obesity-induced changes in adipose tissue macrophage numbers are mainly due to increases in the triple-positive CD11b+ F4/80+ CD11c+ adipose tissue macrophage subpopulation. The ratio of M1-to-M2 macrophages is increased in obesity. Furthermore, hypoxia along with higher concentrations of free fatty acids exacerbates macrophage-mediated inflammation in obesity. The metabolic status of adipocytes is a major determinant of macrophage inflammatory output. Macrophage/adipocyte fatty-acid-binding proteins act at the interface of metabolic and inflammatory pathways. Both macrophages and adipocytes are the sites for active lipid metabolism and signaling.
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PMID:Adipocyte-Macrophage Cross-Talk in Obesity. 2858 6

Hypertrophic white adipose tissue (WAT) represents a maladaptive mechanism linked to the risk for developing type 2 diabetes in humans. However, the molecular events that predispose WAT to hypertrophy are poorly defined. Here, we demonstrate that adipocyte hypertrophy is triggered by loss of the corepressor GPS2 during obesity. Adipocyte-specific GPS2 deficiency in mice (GPS2 AKO) causes adipocyte hypertrophy, inflammation, and mitochondrial dysfunction during surplus energy. This phenotype is driven by HIF1A activation that orchestrates inadequate WAT remodeling and disrupts mitochondrial activity, which can be reversed by pharmacological or genetic HIF1A inhibition. Correlation analysis of gene expression in human adipose tissue reveals a negative relationship between GPS2 and HIF1A, adipocyte hypertrophy, and insulin resistance. We propose therefore that the obesity-associated loss of GPS2 in adipocytes predisposes for a maladaptive WAT expansion and a pro-diabetic status in mice and humans.
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PMID:GPS2 Deficiency Triggers Maladaptive White Adipose Tissue Expansion in Obesity via HIF1A Activation. 3020 20

Obesity is well-known as the second factor for tumorigenesis after smoking and is bound up with the malignant progression of several kinds of cancers, including esophageal cancer, liver cancer, colorectal cancer, kidney cancer, and ovarian cancer. The increased morbidity and mortality of obesity-related cancer are mostly attributed to dysfunctional adipose tissue. The possible mechanisms connecting dysfunctional adipose tissue to high cancer risk mainly focus on chronic inflammation, obesity-related microenvironment, adipokine secretion disorder, and browning of adipose tissue, and so forth. The stromal vascular cells in adipose tissue trigger chronic inflammation through secreting inflammatory factors and promote cancer cell proliferation. Hypertrophic adipose tissues lead to metabolic disorders of adipocytes, such as abnormal levels of adipokines that mediate cancer progression and metastasis. Cancer patients often show adipose tissue browning and cancerous cachexia in an advanced stage, which lead to unsatisfied chemotherapy effect and poor prognosis. However, increasing evidence has shown that adipose tissue may display quite opposite effects in cancer development. Therefore, the interaction between cancers and adipose tissue exert a vital role in mediates adipose tissue dysfunction and further leads to cancer progression. In conclusion, targeting the dysfunction of adipose tissue provides a promising strategy for cancer prevention and therapy.
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PMID:Friend or foe: Multiple roles of adipose tissue in cancer formation and progression. 3105 75


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