Dietary Fibre as a Unifying Remedy for the Whole Spectrum of Obesity-Associated Cardiovascular Risk

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Insulin 17 endocrinologydiseasesdrugs
ezetimibe 1 endocrinologydiseasesdrugs
hyperinsulinemia 1 endocrinologydiseases
hypoglycemia 1 endocrinologydiseases
metabolic syndrome 4 endocrinologydiseases
obesity 24 endocrinologydiseases

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Insulin 20597 fibre effect on body weight regulation mediated by increasing caloric extraction from food [[44]].3. Insulin Resistance, Type 2 Diabetes Risk, and Blood Glucose Control in Diabetes3.1. Epidemiological StudiesTo
Insulin 20874 association between dietary fibre intake and insulin resistance only comes from a secondary analysis of the Insulin Resistance Atherosclerosis Study [[45]]. The results of this US cross-sectional study showed that higher
Insulin 23243 independently of body weight changes as reported in Table 3.3.3. Possible Mechanisms of Fibre Effects on Insulin ResistanceMechanisms underlying the effects of soluble fibre consumption on insulin resistance can be
Insulin 60023 kg/m2HyperinsulinemicWhole-grain products(fibre 28 g/day)vs.refined-grain products(fibre 18 g/day)6↑ Insulin sensitivity(euglycemic hyperinsulinemic clamp tests):+0.07 × 10−4 mmol·kg−1·min−1per pmol/L=
Insulin 60287 F59 years28 kg/m2HealthyRye whole-grain bread(fibre 46 g/day)vs.White wheat bread(fibre 14 g/day)8= Insulin sensitivity(FSIGT)= BWvs.White wheat breadMcIntosh, 2003 [[48]]RCT28 M40–65 years30 kg/m2HealthyRye
Insulin 60506 whole-grain diet(fibre 32 g/day)vs.Wheat whole-grain diet(fibre 32 g/day)vs.Low fibre diet(fibre 19 g/day)4= Insulin resistance (HOMA)= BWvs.Low fibre dietAndersson, 2007 [[49]]RCT30 M/F59 years28.3 kg/m2HealthyWhole-grain
Insulin 60687 years28.3 kg/m2HealthyWhole-grain products(fibre 18 g/day)vs.refined-grain products(fibre 6 g/day)6= Insulin sensitivity (euglycemic hyperinsulinemic clamp tests)↑ BWvs.refined-grain productsKatcher, 2008 [[50]]RCT47
Insulin 60938 syndromeWhole-grain products(fibre 12.9 g/1000 kcal)vs.refined-grain products(fibre 9.7 g/1000 kcal)12= Insulin sensitivity(ISI index during OGTT)↓BWvs.refined-grain productsGiacco, 2010 [[51]]RCT15 M/F55 years27
Insulin 61141 years27 kg/m2HealthyWhole-grain products(fibre 32 g/day)vs.refined-grain products(fibre 20 g/day)3= Insulin resistance (HOMA)= BWvs.refined-grain productsBrownlee, 2010 [[52]]RCT216 M/F46 years30 kg/m2HealthyWhole-grain
Insulin 61342 kg/m2HealthyWhole-grain products(60 g/day)vs.Whole-grain products(120 g/day)vs.refined-grain products16= Insulin sensitivity (QUICKI)= BWvs.refined-grain productsGiacco, 2013 [[53]]RCT133 M/F40–65 years31.4 kg/m2Metabolic
Insulin 61550 kg/m2Metabolic syndromeWhole-grain products(fibre 33 g/day)vs.refined-grain products(fibre 20 g/day)12= Insulin sensitivity(FSIGT)= BWvs.refined-grain productsGiacco, 2014 [[54]]RCT54 M/F40–65 years31.7 kg/m2Metabolic
Insulin 61755 kg/m2Metabolic syndromeWhole-grain products(fibre 33 g/day)vs.refined-grain products(fibre 20 g/day)12= Insulin resistance (HOMA)= BWvs.refined-grain productsFibre from other sourcesHe, 2016 [[55]]Meta-analysis of
Insulin 61997 kg/m2AnyOat-based products(20–136 g/day)vs.β-glucan extract(3–10 g/day)vs.refined-grain products4-12= Insulin resistance (HOMA)= BWvs.refined-grain productsHashizume, 2012 [[56]]RCT30 M/F60.6 years72.5 kg/m2Metabolic
Insulin 62168 [[56]]RCT30 M/F60.6 years72.5 kg/m2Metabolic syndromeResistant maltodextrin(27 g/day)vs.placebo12↓ Insulin resistance (HOMA): −0.5%= BWvs.placeboLi, 2010 [[57]]RCT120M31 years24.5 kg/m2HealthyNUTRIOSE *(27
Insulin 62299 −0.5%= BWvs.placeboLi, 2010 [[57]]RCT120M31 years24.5 kg/m2HealthyNUTRIOSE *(27 g/day)vs.placebo12↓ Insulin resistance (HOMA): −12%↓ BW: −1.5 kgJohnston, 2010 [[58]]RCT20 M/F47.6 years30.8 kg/m2Metabolic
Insulin 62459 2010 [[58]]RCT20 M/F47.6 years30.8 kg/m2Metabolic syndromeResistant starch(40 g/day)vs.placebo12↑ Insulin sensitivity (euglycemic hyperinsulinemic clamp tests tests):+0.9 mg·kg−1·min−1per pmol/L= BWvs.placeboRobertson,
Insulin 62685 2012 [[59]]RCT15 M/F48.9 years33.8 kg/m2Metabolic syndromeResistant starch(40 g/day)vs.placebo8↓ Insulin resistance (HOMA): −0.4%= BWvs.placebo= No significant difference; ↓ significant decrease; ↑ significant
ezetimibe 36198 production that is generally increased in obesity. This was previously shown in a postprandial study with ezetimibe —an intestinal-cholesterol inhibitor—in overweight patients with type 2 diabetes [[106]]. Moreover,
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hyperinsulinemia 44372 postprandial phase [[114]]. Postprandial insulin levels, and more in general, insulin resistance and hyperinsulinemia conditions, may affect blood pressure by increasing renal sodium reabsorption and sympathetic nervous
hypoglycemia 19209 reduction in glucose absorption can also decrease insulin secretion, preventing the risk of reactive hypoglycemia during the post-absorption period and reducing hunger [[34],[35]]. In the small intestine, the role
metabolic syndrome 732 7/2018AbstractObesity is a pandemic carrying the heavy burden of multiple and serious co-morbidities including metabolic syndrome , type 2 diabetes and cardiovascular diseases. The pathophysiological processes leading to the accumulation
metabolic syndrome 1138 blood glucose and lipid metabolism derangement, non-alcoholic fatty liver disease, hypertension, and metabolic syndrome . All these conditions contribute to increase the cardiovascular risk of obese people. Several randomized
metabolic syndrome 3427 [[1]]. The obesity-related burden is mainly carried out by multiple, serious co-morbidities including metabolic syndrome , type 2 diabetes and cardiovascular diseases.The pathophysiological processes leading to the aberrant
metabolic syndrome 35114 relevant reduction of postprandial plasma triglyceride response was also observed in subjects with metabolic syndrome after a 12-week wholegrain rich-diet [[54]]. However, further studies are needed to clarify this issue.4.3.
obesity 1354 randomized clinical trials demonstrated that moderate weight loss (5–10%) in obese patients improves obesity -related metabolic risk factors and coexisting disorders. Therefore, nutritional strategies able to facilitate
obesity 1532 nutritional strategies able to facilitate weight management, and in the meantime positively influence obesity -associated cardiovascular risk factors, should be implemented. To this aim, a suitable option could
obesity 2555 Although the evidence is not conclusive, this suggests that fibre would be a suitable option to counteract obesity -related cardio-metabolic diseases also independently of weight loss. However, evidence is not consistent
obesity 3336 pandemic currently involving 600 million adults and 40 million children prior to 5 years of age [[1]]. The obesity -related burden is mainly carried out by multiple, serious co-morbidities including metabolic syndrome,
obesity 4938 adipose tissue, which contributes to the insulin resistance that is often present in patients with obesity [[3],[4]].The threshold saturation of subcutaneous adipose tissue is mainly genetically determined and
obesity 8981 randomized clinical trials demonstrated that moderate weight loss (5–10%) in obese patients improves obesity -related metabolic risk factors and coexisting disorders [[16],[17],[18]]. Therefore, nutritional strategies
obesity 9274 strategies may need qualitative dietary modifications that could favorably affect mechanisms behind obesity and associated cardiometabolic risk factors development. Increasing the consumption of dietary fibre
obesity 9595 current evidence on the effects of dietary fibres on (a) weight management in obese people and (b) obesity -associated cardio-metabolic diseases. We have comprehensively examined the evidence from observational
obesity 10361 relevant reference trials. We used as keywords “detary fibre OR fibre” and separate search terms for obesity and each of the cardiovascular risk factors. The search yielded 531 articles for “obesity OR weight
obesity 10453 terms for obesity and each of the cardiovascular risk factors. The search yielded 531 articles for “ obesity OR weight management OR waist circumference OR body weight OR abdominal obesity”, 397 articles for
obesity 10533 531 articles for “obesity OR weight management OR waist circumference OR body weight OR abdominal obesity ”, 397 articles for “insulin resistance OR blood glucose OR diabetes risk”, 577 articles for “dyslipidemia
obesity 15730 weeks. In a “review of meta-analyses” [[32]], the reductions in body weight, BMI, and abdominal obesity observed in individuals with the highest dietary whole grain intake were not significantly different
obesity 24134 resistance [[63]].However, the prebiotic effect of fibre may also play a role. It has been observed that obesity -related dysbiosis may lead to the development of insulin resistance [[64],[65]]. Several studies have
obesity 31452 insulin resistance—i.e., the main pathophysiological process leading to blood glucose disruption in obesity (Figure 1), and on blood glucose control, the consumption of foods rich in fibre should be encouraged
obesity 31658 encouraged to prevent or improve blood glucose metabolism derangement that typically occurs in people with obesity .4. Dyslipidaemia4.1. Epidemiological StudiesTwo epidemiological studies met the study’s inclusion
obesity 36134 lipoproteins/remnants—by reducing substrate availability for hepatic lipoprotein production that is generally increased in obesity . This was previously shown in a postprandial study with ezetimibe—an intestinal-cholesterol inhibitor—in
obesity 36589 reduces the small and dense LDL fraction that is increased in all insulin-resistant states including obesity [[107]].As for the effects on postprandial triglycerides, it has been suggested that dietary fibre slows
obesity 37228 lipoproteins is a main pathway through which dietary fibres disrupt deleterious mechanisms leading to obesity -related atherogenic dyslipidaemia.4.4. ConclusionsSoluble/high fermentable fibre intake represents an
obesity 37681 fibre. Very few data are available for other components of atherogenic dislipidemia associated with obesity : high triglyceride and low HDL cholesterol levels.5. Blood Pressure/Hypertension5.1. Epidemiological
obesity 45711 weight reduction, on specific pathophysiological mechanisms leading to hypertension development in obesity .6. Non Alcoholic Fatty Liver Disease6.1. Epidemiological StudiesEpidemiological studies, in particular
obesity 52725 which dietary fibre may act on individual cardiovascular risk factors, i.e., hypertension, central obesity , insulin resistance, and dyslipidemia, which have been discussed in detail in the above paragraphs.
obesity 53815 beneficially influence all parameters of body weight management and metabolic disorders related to obesity with consequent advantages on global cardiovascular risk.Evidence strength varies among metabolic conditions
obesity 55631 and hepatic insulin resistance acts on a key metabolic crossway from which the pathogenesis of all obesity -associated cardiovascular risk starts. Each of these effects differently influences cardio-metabolic
obesity 55939 approach including foods containing all types of fibre would be suitable to globally prevent and treat obesity and related disorders.Although many of the nutritional studies reported above were designed to induce

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