Obesity-Related Digestive Diseases and Their Pathophysiology

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Term Occurence Count Dictionary
Insulin 3 endocrinologydiseasesdrugs
diabetes mellitus 4 endocrinologydiseases
metabolic syndrome 8 endocrinologydiseases
metformin 3 endocrinologydiseasesdrugs
obesity 70 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
Insulin 3198 1 (IGF-1) bioavailability and inhibit apoptosis and increase cell proliferation on target cells.1. Insulin and IGFsObesity is strongly related with insulin resistance, in which insulin and IGF-1 are elevated
Insulin 3491 receptor signaling pathways are known to be related with the formation of many kinds of cancer.[7] Insulin induced proliferation of colon cancer cells in vitro,[8] while IGF-1 inhibits apoptosis, leading to
Insulin 3873 women.[10],[11] High serum C-peptide, a marker for insulin production, increased colorectal cancer risk.[12] Insulin increased IGF-1 that binds to IGF-1 receptor and insulin receptor. After IGF-1 binds IGF-1 receptor,
metformin 4348 signal-regulated kinase (ERK) pathway that induces cell proliferation.A previous study suggested that metformin , oral antihyperglycemic agent, may reduce the risk of cancer.[13] One of suggested anticancer mechanisms
metformin 4466 antihyperglycemic agent, may reduce the risk of cancer.[13] One of suggested anticancer mechanisms of metformin is the inhibition of the mTORC1.[14] The mTOR signaling network plays a pivotal role in metabolism and
metformin 4663 metabolism and proliferation of cancer cell.[15] The reduction of circulating insulin and IGF-1 by metformin may be associated with anticancer action.[16]2. AdipokinesAdipokines are cytokines released from adipose
Select Disease Character Offset Disease Term Instance
diabetes mellitus 21787 fibrosis.[129],[130]2. Advanced hepatitis C-related diseaseThe presence of hepatic steatosis, along with obesity and diabetes mellitus , seems to increase the risk of HCC in chronic HCV. Hepatic steatosis is one of established histopathologic
diabetes mellitus 22547 (HR, 3.10) as compared to underweight patients.[136] Another Japanese cohort study demonstrated that diabetes mellitus , based on a positive 75 g oral glucose tolerance test, increased the risk of HCC development in chronic
diabetes mellitus 22894 HCV.[138]3. Cirrhosis and HCCSeveral epidemiologic studies have suggested the possible link between diabetes mellitus and HCC.[139],[140] Many patients with diabetes have NAFLD, a risk factor for HCC. It seems that NAFLD
diabetes mellitus 24135 the risk of gallbladder cancer.[144]Several epidemiologic studies suggested an association between diabetes mellitus and cholangiocarcinoma. A meta-analysis using 15 studies demonstrated that patients with diabetes had
metabolic syndrome 18031 measured by BMI and colorectal cancer,[98],[99] recent studies suggested that abdominal obesity and metabolic syndrome were stronger predictors of colorectal adenoma than BMI, a marker of general obesity.[100],[101] Visceral
metabolic syndrome 19174 colorectal adenoma had a dose-response correlation with VAT in both sexes, whereas it was related with metabolic syndrome , BMI, and waist circumference in men but not in women.[4] Women seem to accumulate less VAT with weight
metabolic syndrome 21201 severe fibrosis or cirrhosis.[123]–[125] NAFLD is also strongly associated with insulin resistance and metabolic syndrome .[126],[127] Among individuals with NAFLD, about 90% have features of metabolic syndrome.[128]The development
metabolic syndrome 21289 resistance and metabolic syndrome.[126],[127] Among individuals with NAFLD, about 90% have features of metabolic syndrome .[128]The development of NAFLD is known to be through a “two hit” process.[129],[130] The first “hit”
metabolic syndrome 23379 etiology.[141] HCC may be a late complication of NASH-induced cirrhosis. NAFLD, the predominant manifestation of metabolic syndrome in the liver can progress to cirrhosis and HCC.[142] Metformin decreases HCC risk in a dose-dependent
metabolic syndrome 27785 and poor stool consistency.METABOLIC AND MEDICAL EFFECT OF WEIGHT REDUCTIONWeight reduction improved metabolic syndrome and insulin resistance and subsequently may reduce the risk of obesity-related benign diseases.[156],[157]
metabolic syndrome 31981 diseases. Obesity increases free fatty acids and alters adipocy-tokines. This metabolic alteration induces metabolic syndrome , including insulin resistance, dyslipidemia, and hypertension. Metabolic alteration and metabolic syndrome
metabolic syndrome 32088 metabolic syndrome, including insulin resistance, dyslipidemia, and hypertension. Metabolic alteration and metabolic syndrome contribute to benign and malignant digestive disease. Mechanical effect of obesity may contribute to
obesity 267 11/2016AbstractObesity is a growing medical and public health problem worldwide. Many digestive diseases are related to obesity . In this article, the current state of our knowledge of obesity-related digestive diseases, their pathogenesis,
obesity 331 Many digestive diseases are related to obesity. In this article, the current state of our knowledge of obesity -related digestive diseases, their pathogenesis, and the medical and metabolic consequences of weight
obesity 759 C-related disease, hepatocellular carcinoma, gallstone, cholangiocarcinoma, and pancreatic cancer. Although obesity -related esophageal diseases are associated with altered mechanical and humoral factors, other obesity-related
obesity 861 obesity-related esophageal diseases are associated with altered mechanical and humoral factors, other obesity -related digestive diseases seem to be associated with obesity-induced altered circulating levels of
obesity 923 mechanical and humoral factors, other obesity-related digestive diseases seem to be associated with obesity -induced altered circulating levels of adipocytokines and insulin resistance. The relationship between
obesity 1073 adipocytokines and insulin resistance. The relationship between functional gastrointestinal disease and obesity has been debated. This review provides a comprehensive evaluation of the obesity-related digestive diseases,
obesity 1154 gastrointestinal disease and obesity has been debated. This review provides a comprehensive evaluation of the obesity -related digestive diseases, including pathophysiology, obesity-related risk, and medical and metabolic
obesity 1217 provides a comprehensive evaluation of the obesity-related digestive diseases, including pathophysiology, obesity -related risk, and medical and metabolic effects of weight reduction in obese subjects.INTRODUCTIONThe
obesity 1348 medical and metabolic effects of weight reduction in obese subjects.INTRODUCTIONThe prevalence of global obesity among both women and men increased from 1980 to 2008 (Fig. 1).[1] With a new appreciation for obesity
obesity 1450 obesity among both women and men increased from 1980 to 2008 (Fig. 1).[1] With a new appreciation for obesity as a disease and well-being in mind, the concerns of obesity and obesity-related disease have been rapidly
obesity 1511 (Fig. 1).[1] With a new appreciation for obesity as a disease and well-being in mind, the concerns of obesity and obesity-related disease have been rapidly increased. The health implications by obesity include
obesity 1523 With a new appreciation for obesity as a disease and well-being in mind, the concerns of obesity and obesity -related disease have been rapidly increased. The health implications by obesity include a wide spectrum
obesity 1603 concerns of obesity and obesity-related disease have been rapidly increased. The health implications by obesity include a wide spectrum of benign digestive diseases such as gastroesophageal reflux disease (GERD),
obesity 2172 common adverse treatment effects in cancer patient.[6]Both mechanical effect and humoral factors by obesity seem to effect on development of esophageal diseases, whereas pathophysiology of other digestive disorders
obesity 2312 esophageal diseases, whereas pathophysiology of other digestive disorders seems to be related with obesity induced proinflammatory and inflammatory cytokines. The relationship of functional gastrointestinal
obesity 2433 proinflammatory and inflammatory cytokines. The relationship of functional gastrointestinal disease with obesity has debate.This review provides gastroenterologists with a comprehensive evaluation of the obesity-related
obesity 2532 obesity has debate.This review provides gastroenterologists with a comprehensive evaluation of the obesity -related digestive diseases, including pathophysiology of carcinogenesis, obesity-related risk of each
obesity 2613 evaluation of the obesity-related digestive diseases, including pathophysiology of carcinogenesis, obesity -related risk of each disease, and medical effect of weight reduction.PATHOPHYSIOLOGY OF CARCINOGENESIS
obesity 11332 ImmuomodulationObesity is associated with low-grade inflammation. Chronic inflammation associated with obesity modulates immune cell function.[57] Epithelial γδ T cell function is the guardians of the epithelial
obesity 11878 fatty acids were the most prominent modulators of T-cell proliferation. T-cell co-stimulation protects obesity -induced adipose inflammation and insulin resistance.[60]The amount of adipocytokines produced by adipose
obesity 12679 for GERDs in both Asian and Western.[64],[65] Large epidemiological studies have demonstrated that obesity is an important risk factor of GERD.[64]–[66] Jacobson et al.[65] showed that subjects that reported
obesity 13327 453 hospital employees responded GERD symptom questionnaires and 196 subjects underwent endoscopy, obesity was associated with reflux symptoms and esophagitis.[67]Abdominal visceral adiposity, rather than BMI,
obesity 13661 comprehensive screening individuals demonstrated that odds ratio (OR) for erosive esophagitis correlated with obesity measured by BMI, waist circumference, and abdominal visceral adipose tissue volume (p<0.001 for each
obesity 14051 compared with participants who had visceral adipose tissue volumes less than 500 cm3.[3] When all three obesity indexes were analyzed simultaneously, abdominal visceral adipose tissue volume, but not BMI or waist
obesity 14250 or waist circumference, was associated with erosive esophagitis.[3]Pathophysiological mechanism in obesity include lower esophageal sphincter abnormalities, increased risk of hiatal hernia, and increased intragastric
obesity 14490 Additionally, alterations in the secretion of adiponectin and leptin from adipocytes is a proposed link between obesity and Barrett’s esophagus and EAC.The data for weight reduction as a treatment for GERD is less robust,
obesity 15383 has shown to decrease GERD symptoms.[71]–[73]2. Barrett’s esophagus and esophageal cancerGERD and obesity are strong risk factors of EAC and BE. A landmark population-based case-control study showed that the
obesity 16346 associated with a 2.4-fold increase in risk of EAC compared with a BMI of less than 25 kg/m2.[80] Abdominal obesity is associated with BE and EAC (OR, 2.51).[81] A recent Mendelian randomized study using 999 patients
obesity 16773 and promoted formation of hiatal hernia, which is a strong risk factor of GERD.[83],[84] Abdominal obesity is associated with BE and EAC after adjusting for GERD.[80] In addition to mechanical effect, abdominal
obesity 16885 associated with BE and EAC after adjusting for GERD.[80] In addition to mechanical effect, abdominal obesity changed circulating levels of inflammatory cytokines that are associated with BE and EAC.[85] Metabolic
obesity 17267 in IGF-I gene is associated with BE,[89] and a polymorphism in IGF-I receptor modifies the effect of obesity on the risk of BE and EAC.[90] The IGF pathway is also involved in the risk of progression from BE to
obesity 17682 and progression to EAC in some, but not all, studies.[85],[92],[94],[95] Complex metabolic effects of obesity seem to have synergistic effects with GERD on the risk of BE and EAC.[96],[97]COLORECTAL ADENOMA AND
obesity 17923 risk factor for colorectal adenoma and cancer. Previous studies showed a positive association between obesity measured by BMI and colorectal cancer,[98],[99] recent studies suggested that abdominal obesity and
obesity 18019 between obesity measured by BMI and colorectal cancer,[98],[99] recent studies suggested that abdominal obesity and metabolic syndrome were stronger predictors of colorectal adenoma than BMI, a marker of general
obesity 18127 and metabolic syndrome were stronger predictors of colorectal adenoma than BMI, a marker of general obesity .[100],[101] Visceral adipose tissue (VAT) is associated with insulin resistance and higher circulating
obesity 19376 less VAT with weight gain than men.[3],[110]Large prospective cohort studies have demonstrated that obesity increases the risk of colorectal cancer by 1.5-fold compared to normal weight persons.[111] However,
obesity 19638 BMI and CRC.[112] In sex-specific meta-analysis, the incidence of colorectal cancer was higher with obesity , with relative risk (RR) varying from 1.37 to 1.95 for CRC in men, whereas the association between obesity
obesity 19745 obesity, with relative risk (RR) varying from 1.37 to 1.95 for CRC in men, whereas the association between obesity and CRC was weaker in women.[113]–[115] The incidence of CRC was higher in women with obesity in two
obesity 19841 between obesity and CRC was weaker in women.[113]–[115] The incidence of CRC was higher in women with obesity in two of the three studies (RR, 1.15).[114]–[116] A pooled analysis using 300,000 Japanese subjects
obesity 21775 fibrosis.[129],[130]2. Advanced hepatitis C-related diseaseThe presence of hepatic steatosis, along with obesity and diabetes mellitus, seems to increase the risk of HCC in chronic HCV. Hepatic steatosis is one of
obesity 22273 a Japanese cohort study consisted of 1,431 patients with chronic HCV following for up to 10 years, obesity is an independent risk factor for HCC development in chronic HCV.[136] The risk of HCC in chronic HCV
obesity 22725 increased the risk of HCC development in chronic HCV.[137] NAFLD and its associated risk factors such as obesity and diabetes increase the risk of HCC development in chronic HCV.[138]3. Cirrhosis and HCCSeveral epidemiologic
obesity 23825 gallstone-related complications and cholecystectomy. Clinical and epidemiological studies have suggested that obesity is positively related with the risk of gallbladder cancer. Obesity may modulate lipid and endogenous
obesity 25265 cancer at a younger age than persons with a normal weight.[149]GASTRIC CANCERThe association between obesity and gastric cancer has not been well studied. A meta-analysis from 10 studies with 9,492 gastric cancer
obesity 25426 meta-analysis from 10 studies with 9,492 gastric cancer and 3,097,794 total population demonstrated that obesity (BMI>25) was associated with an increased risk of gastric cancer (OR, 1.22).[151] In stratified analysis,
obesity 25540 (BMI>25) was associated with an increased risk of gastric cancer (OR, 1.22).[151] In stratified analysis, obesity (BMI>25) was associated with an increased risk of cardia gastric cancer (OR, 1.55) and gastric cancer
obesity 25879 from 24 prospective studies with 41,791 cases demonstrated that both overweight (BMI, 25 to 30) and obesity (BMI≥30) were not associated with risk of total gastric cancer.[152] However, BMI was positively associated
obesity 26103 the risk of gastric cardia cancer but not with gastric noncardia cancer. These results indicate that obesity is related with cardiac cancer but not with noncardiac cancer.FUNCTIONAL GASTROINTESTINAL DISEASEMeta-analysis
obesity 26289 GASTROINTESTINAL DISEASEMeta-analysis of 21 studies comprising data from 77,538 individuals demonstrated obesity increased the risk of upper abdominal pain (OR, 2.65), gastroesophageal reflux (OR, 1.89), diarrhea
obesity 26677 bloating, constipation/hard stools, fecal incontinence, nausea and anal blockage had no association with obesity .[153]For Australian adults, the prevalence of 26 gastrointestinal symptoms was determined by a validated
obesity 26914 which was sent to 5,000 randomly selected residents.[154] The response rate was 60%. The prevalence of obesity (BMI≥30 kg/m2) and overweight was 25.1% and 36.1%, respectively. The adjustment for socioeconomic
obesity 27245 1.35), and diarrhea (OR, 1.86), whereas dysmotility symptoms and constipation had no association with obesity .[154] Of 3,927 invited subjects, 1,731 (44.1%) responded to the questionnaire to assess the occurrence
obesity 27451 occurrence of functional bowel (FB) symptoms in Northern Norway.[155] In a multivariate regression model, obesity increased the risk of FB (OR, 1.61).[155]Upper abdominal pain may be related to postprandial stomach
obesity 27867 reduction improved metabolic syndrome and insulin resistance and subsequently may reduce the risk of obesity -related benign diseases.[156],[157] Many observational studies have shown that people who have a lower
obesity 28405 for cancer prevention in world-wide.Obesity also may contribute to poor prognosis and low survival in obesity -related cancer patients. Weight reduction by bariatric surgery appear to reduce obesity-related benign
obesity 28493 survival in obesity-related cancer patients. Weight reduction by bariatric surgery appear to reduce obesity -related benign disease and cancers in extreme obese perosons.[158]–[160] Also bariatric surgery in
obesity 28718 patients reduced all-cause and cause-specific mortality.[161] The high effect of Bariatric surgery on obesity -related medical condition may be below; whereas most lifestyle modification result in weight reduction
obesity 29281 cohort study of 25,291 colon cancer patients who received treatment in adjuvant chemotherapy trials, obesity and underweight status were associated independently with inferior outcomes.[163] Recent meta-analysis
obesity 29424 associated independently with inferior outcomes.[163] Recent meta-analysis using eight studies showed that obesity is associated with poorer overall and breast cancer survival in pre- and post-menopausal breast cancer.[164]Several
obesity 30284 intentional weight reduction has been recommended as one of the important life style modification in obesity -related cancers.CONCLUSIONSOverweight and obesity, particularly abdominal visceral obesity, increased
obesity 30334 as one of the important life style modification in obesity-related cancers.CONCLUSIONSOverweight and obesity , particularly abdominal visceral obesity, increased the risk of a wide spectrum of benign digestive
obesity 30375 modification in obesity-related cancers.CONCLUSIONSOverweight and obesity, particularly abdominal visceral obesity , increased the risk of a wide spectrum of benign digestive diseases such as GERD, BE, erosive esophagitis,
obesity 30693 pancreatic cancer, colorectal cancer, and esophageal cancer.Both mechanical and humoral factors caused by obesity seem to be involved in the development of esophageal diseases, whereas pathophysiology of other digestive
obesity 30842 esophageal diseases, whereas pathophysiology of other digestive disorders seems to be related with obesity induced proinflammatory and inflammatory cytokines. Excessive weight and adiposity induce increase of
obesity 31263 weight reduction can improve the insulin resistance and subsequently seems to reduce the incidence of obesity -related cancer and mortality.Fig. 1Estimates of obesity prevalence in women (A) and men (B). Among women,
obesity 31319 subsequently seems to reduce the incidence of obesity-related cancer and mortality.Fig. 1Estimates of obesity prevalence in women (A) and men (B). Among women, obesity prevalence has increased in all regions. The
obesity 31377 obesity-related cancer and mortality.Fig. 1Estimates of obesity prevalence in women (A) and men (B). Among women, obesity prevalence has increased in all regions. The greatest magnitudes of increase (>20%) were observed in
obesity 31568 were observed in central Latin America, North America, North Africa, and the Middle East. For men, obesity has increased in all regions except South Asia. The greatest magnitude of increase was observed in North
obesity 31853 Endocrinol 2013;9:13–27, with permission from Nature Publishing Group.[1]Fig. 2Medical effect of obesity on digestive diseases. Obesity increases free fatty acids and alters adipocy-tokines. This metabolic
obesity 32182 alteration and metabolic syndrome contribute to benign and malignant digestive disease. Mechanical effect of obesity may contribute to esophageal disease and several gastrointestinal symptoms.GERD, gastroesophageal reflux

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