The Metabolic Syndrome: A Concept Hard to Define

Aguilar-Salinas, Carlos A.; Rojas, Rosalba; Gómez-Pérez, Francisco J.; Mehta, Roopa; Franco, Aurora; Oláiz, Gustavo; Rull, Juan

doi:10.1016/j.arcmed.2004.12.003

Cited by 72 publications

(50 citation statements)

References 39 publications

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“…Presently, there is no universally accepted definition of the MetS. 32 Studies on the association with colorectal cancer risk used different MetS factors and cut-off points, which somewhat complicates comparisons between studies. Nevertheless, four out of five previous prospective studies (excluding a very small study of 54 cases 26 ), consistently reported a 1.4-1.5-fold significant increased risk of incident or fatal colorectal cancer in subjects with three or more MetS factors present (Table 5).…”

Section: Discussionmentioning

confidence: 99%

Components of the metabolic syndrome and colorectal cancer risk; a prospective study

et al. 2007

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Objective: To examine the relation of well-known factors of the metabolic syndrome (MetS) as well as related circulating factors, with risk of colorectal cancer. Methods: We performed a case control study of 306 colorectal cancer cases and 595 matched controls nested in the Northern Sweden Health and Disease Cohort. Levels of C-peptide, glycated haemoglobin (HbA1c), leptin and adiponectin were measured in cryopreserved samples. Body mass index (BMI), systolic and diastolic blood pressure and fasting and post-load plasma glucose, had been measured in a subcohort. Conditional logistic regression was used to calculate odds ratios (OR) of disease, including risk assessments for the MetS factors: obesity (BMI430 kg m À2 ), hypertension (blood pressure X140/90 mmHg or use of anti-hypertensive drugs) and hyperglycaemia (fasting glucose X6.1 mmol l À1 or post-load glucose in capillary plasma X8.9 mmol l À1 ). Results: None of the studied variables were significantly associated with risk across quartiles. Presence of obesity, hypertension and hyperglycaemia significantly increased the risk of colorectal cancer; OR for three vs null factors was 2.57 (95% Confidence Interval [CI] 1.20-5.52; P trend ¼ 0.0021), as compared to a 30 to 70% increased risk for the factors in single. Similarly, top decile levels of C-peptide, HbA1c and leptin/adiponectin ratio were associated with an increased risk; ORs for top vs deciles 1-9 were 1.56 (95% CI 0.93-2.62; P ¼ 0.090), 1.83 (95% CI 1.00-3.36; P ¼ 0.051) and 1.50 (95% CI 0.83-2.71; P ¼ 0.18), respectively. Conclusions: Our study support the view that components of the MetS increase risk of colorectal cancer, and further suggests that only very high levels of metabolic factors confer an increased risk.

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Section: Discussionmentioning

confidence: 99%

Components of the metabolic syndrome and colorectal cancer risk; a prospective study

et al. 2007

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“…6 The metabolic syndrome has been defined using harmonized guidelines requiring presence of >3 of the following risk factors: Waist circumference >88 cm, triglycerides >150 mg/dl, HDL cholesterol <50 mg/dl, systolic blood pressure (BP) >130 or diastolic BP >85mmHg, or treatment of previously diagnosed hypertension, and fasting plasma glucose >100 mg/dl. 7 The potential biological link between the endometrial cancer and metabolic syndrome is incompletely understood and the mediators for this association are not known, but are thought to be related to hyperinsulinemia (either due to insulin resistance or due to administered insulin), hyperglycaemia, insulin like-growth factor, and adipocytokines. 8 Moreover, evidence from observational studies suggests that some oral glucose lowering medications used to treat hyperglycaemia are associated with either increased or reduced cancer risk or mortality.…”

Section: Introductionmentioning

confidence: 99%

The impact of metabolic syndrome on the clinical profile and tumor characteristics of endometrial carcinoma

Tawfik

ElSabaa

Elneily

et al. 2016

Int J Reprod Contracept Obstet Gynecol

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“…There is a general consensus that the rising prevalence of obesity, type II diabetes and its essential prerequisite, insulin resistance, is related to consumption of these processed and calorie-dense foods, rich in saturated fat and carbohydrates with a high glycaemic index (Bayol et al 2005;Fulgoni, 2008). Diet-induced obesity is a major risk factor for development of the metabolic syndrome, a disorder characterized by impaired glucose tolerance, hyperuricaemia, hypertriglyceridaemia and hypertension, and which is considered to be prediabetic (Aguilar-Salinas et al 2005;Junien & Nathanielsz, 2007;AlSaraj et al 2009). Increased consumption of saturated and trans-saturated fats and carbohydrates has also been shown to have an adverse effect on glucose metabolism and induce insulin resistance (Moeller et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Experimental type II diabetes and related models of impaired glucose metabolism differentially regulate glucose transporters at the proximal tubule brush border membrane

Chichger

Cleasby

Srai

et al. 2016

Experimental Physiology

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New Findings r What is the central question of this study?Although SGLT2 inhibitors represent a promising treatment for patients suffering from diabetic nephropathy, the influence of metabolic disruption on the expression and function of glucose transporters is largely unknown. r What is the main finding and its importance?In vivo models of metabolic disruption (Goto-Kakizaki type II diabetic rat and junk-food diet) demonstrate increased expression of SGLT1, SGLT2 and GLUT2 in the proximal tubule brush border. In the type II diabetic model, this is accompanied by increased SGLT-and GLUT-mediated glucose uptake. A fasted model of metabolic disruption (high-fat diet) demonstrated increased GLUT2 expression only. The differential alterations of glucose transporters in response to varying metabolic stress offer insight into the therapeutic value of inhibitors. SGLT2 inhibitors are now in clinical use to reduce hyperglycaemia in type II diabetes. However, renal glucose reabsorption across the brush border membrane (BBM) is not completely understood in diabetes. Increased consumption of a Western diet is strongly linked to type II diabetes. This study aimed to investigate the adaptations that occur in renal glucose transporters in response to experimental models of diet-induced insulin resistance. The study used Goto-Kakizaki type II diabetic rats and normal rats rendered insulin resistant using junk-food or high-fat diets. Levels of protein kinase C-βI (PKC-βI), GLUT2, SGLT1 and SGLT2 were determined by Western blotting of purified renal BBM. GLUT-and SGLT-mediated d-[3 H]glucose uptake by BBM vesicles was measured in the presence and absence of the SGLT inhibitor phlorizin. GLUT-and SGLT-mediated glucose transport was elevated in type II diabetic rats, accompanied by increased expression of GLUT2, its upstream regulator PKC-βI and SGLT1 protein. Junk-food and high-fat diet feeding also caused higher membrane expression of GLUT2 and its upstream regulator PKC-βI. However, the junk-food diet also increased SGLT1 and SGLT2 levels at the proximal tubule BBM. Glucose reabsorption across the proximal tubule BBM, via GLUT2, SGLT1 and SGLT2, is not solely dependent on glycaemic status, but is also influenced by

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The Metabolic Syndrome: A Concept Hard to Define

Cited by 72 publications

References 39 publications

Components of the metabolic syndrome and colorectal cancer risk; a prospective study

Components of the metabolic syndrome and colorectal cancer risk; a prospective study

The impact of metabolic syndrome on the clinical profile and tumor characteristics of endometrial carcinoma

Experimental type II diabetes and related models of impaired glucose metabolism differentially regulate glucose transporters at the proximal tubule brush border membrane

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