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dried potatoes, vegetable oil, corn flower, wheat starch, maltodextrin, salt, and my favorite ingredient of all, uniformity.
بطاطس مجففة ، زيت نباتي ،زهرة الذرة نشا القمح ، مواد نشوية ،الملح والمكون المفضّل لي من بينهم جميعا التناسق بينهم
2.5. gut and gut microbiota the gut plays central roles in the processing of carbohydrates and thereby influences glucose balance in the body (fig. 1a). gut endocrine functions and the gut bacterial population (microbiota) are emerging key players in the regulation of intermediary meta- bolism. unfavorable microbiota may contribute to the onset of obesity and metabolic syndrome mainly by triggering pro- inflammatory responses, and by favoring efficient nutrient ab- sorption [60,61]. on the other hand, beneficial bacterial strains may result in protection from metabolic disease, and interaction with non-digestible dietary carbohydrates contributes to this effect. in particular, dietary fibers interact with the gut microbiota and may reduce inflammation and unfavorable metabolic responses, thereby also reducing hepatic steatosis [41,62]. gut microbiota- driven fermentation of non-digestible carbohydrates or prebiotics can decrease carbohydrate-induced blood glucose spikes that occur after a meal [63]. probiotics may further modulate release of gut peptides including glucagon-like peptide 1 (glp-1), also potentially contributing to limit obesity and its metabolic complications (45, 82). fermentation of non-digestible carbohydrates also results in production of short chain fatty acids (scfas) that may play pro- tective roles and reduce the risk for systemic and local disease including cancer. obese individuals are reported to display meta- bolically unfavorable populations of gut microbes, and weight loss after gastric bypass surgery may shift this pattern towards one resembling normal weight individuals [64,65]. the possibility of harnessing microbiota to treat obesity and metabolic disease is under intensive investigation. small-scale clinical studies of pro- biotic supplementation have found favorable changes to glucose and fat metabolism [61,66e68]. research has identified metaboli- cally beneficial bacterial strains in the gut microbiota, like lacto- bacillus, and bifidobacterium, or akkermansia, though their role as modulators of the host metabolism is still debated [69,70]. larger and longer-term human trials are still necessary before tailored probiotic use can be incorporated into official guidelines for the treatment of obesity and metabolic syndrome [61,71]. 2.6. fructose glucose is the body's key form of energy and the most clinically relevant carbohydrate employed in patient nutritional support. for these reasons, glucose is the main focus of the current review. however, glucose is not the only simple sugar available through the diet. fructose (as a monosaccharide or in the disaccharide sucrose) is also found in a variety of foods, but is processed differently by the body. fructose has also been a focus of research, as it not only enters the diet through fruits but also is added to juices and other food products as a sweetener, and therefore is widely consumed. after absorption, fructose is metabolized by the liver and can be con- verted into glucose, lactate, and fatty acids. fructose-induced he- patic lactate release is a unique feature and opposite to extrahepatic lactate flux to the liver for de novo glucose production. high- fructose diets have been reported to decrease insulin-mediated suppression of glucose production and to increase hepatic lipo- genesis and plasma triglyceride concentrations [72], although recent meta-analyses have failed to confirm associations between fructose intake and several metabolic alterations potentially due to additional adaptive changes [73]. as introduced above, a stronger link has been established between fructose and non-alcoholic fatty liver disease (nafld), involving stimulation by fructose ingestion of pro-inflammatory signals reaching the liver from the gut [44,46,74]. ingestion of a fructose-free diabetes-specific nutrition supplement formula (dsf) was shown to cause lower blood glucose concen- trations in patients with diabetes than formulas with fructose [75], and physical activity has been shown to attenuate its deleterious effects on glycemic control [76]. however, as these effects of fruc- tose are still debated [73], additional trials to determine whether fructose in particular should be avoided in the diet are necessary. 3. recommendations for glycemic management and nutritional support 3.1. obesity, metabolic syndrome, and diabetes 3.1.1. diet and lifestyle obesity and excess adiposity can lead to the development of glucose insensitivity, impaired insulin action, and inability to properly regulate glycemic variations. although dietary recom- mendations aimed at weight loss have recently emphasized the importance of inducing energy deficits, at least in part indepen- dently of diet composition, high gi and gl foods are associated with metabolic disease risk and health complications [3e5]. lowering dietary gi and gl may conversely improve these outcomes and benefit patients with obesity and diabetes [6e11]. non-digestible carbohydrates may also provide beneficial metabolic effects. solu- ble fiber is reported to decrease postprandial plasma glucose con- centration and it may additionally decrease blood ldl-cholesterol concentration [7,77]. insoluble fiber, especially cereal fiber, de- creases the risk of t2d and cardiovascular disease [78]. high fiber intake is therefore recommended for people with diabetes or at risk of developing diabetes, including people with obesity and meta- bolic syndrome (i.e. the cluster of cardiometabolic risk factors including high waist circumference, high blood pressure, elevated blood glucose and dyslipidemia with high triglycerides and low hdl-cholesterol). such nutritional recommendations (tables 1 and 2) have been increasingly introduced by several health care orga- nizations and are currently included in guidelines for patients with or at risk of developing t2d, and they are also appropriate for the management of plasma glucose concentration in type 1 diabetes (t1d) [79e81]. 3.1.2. disease-specific nutritional supplement formulas for diabetes nutritional support can cause or exacerbate hyperglycemia, especially in obese and diabetic patients, and hyperglycemia is associated with higher morbidity and mortality [91,92]. in the clinical nutrition setting, a burgeoning field of research is dedicated to designing nutritional support products for people with diabetes. such products aim to limit glycemic variation after administration [93]. diabetes-specific formulas (dsf) have many of the following ingredients in common: a) lower carbohydrate content than stan- dard formulas (sfs); b) higher proportion of complex carbohydrates that are slowly digestible to reduce blood glucose spiking; c) modified maltodextrin, starch, fructose, isomaltulose, and sucro- malt, rather than the maltodextrin, starch, and sucrose found in sfs [94]; d) fat content enriched in unsaturated fatty acids, especially monounsaturated fatty acids, in higher proportion than in sfs [87]; e) fiber content higher than in sfs [95]. based on this available evidence, the espen expert group en- dorses the utilization of dsfs for nutritional support of people with obesity and diabetes. when parenteral nutrition must be used, the risk of hyperglycemia in obese and diabetic patients can be reduced if the initial amounts of glucose provided in the tpn bag are limited to less than 2 g/kg/day until proper glycemic control is observed [96]. with the use of enteral nutrition, the risk of hyperglycemia can be decreased by modification of the total amount and of the quality of carbohydrates used. numerous short- and mid-term studies prove that enteral dsfs are associated with reduced post- prandial blood glucose, postprandial blood insulin, mean blood glucose values, glycemic variability, short-acting insulin
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