Abstract

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Dietary Carbohydrates in the Prevention

and Treatment of Metabolic Diseases

Wpływ węglowodanów w diecie na profilaktykę

i przebieg chorób metabolicznych

Department of Food Science and Nutrition, Silesian Piasts University of Medicine in Wrocław, Poland

Adv Clin Exp Med 2007, 16, 4, 577–588 ISSN 1230−025X

REVIEWS

© Copyright by Silesian Piasts University of Medicine in Wrocław

Abstract

Diets based on the glycemic index (GI) were developed for the first time in the early 1980s. The glycemic index ranks carbohydrate−containing foods according to their impact on postprandial glycemia. Ingestion of high− glycemic−index products (most highly processed foods containing starch in the form of amylopectin and simple sugars) may raise the risk of metabolic disease by inducing insulin resistance. Low−glycemic−index diets, in con− trast, contribute to a rise in insulin sensitivity. Constant presence of high postprandial glycemia (above 140 mg/dl two hours after a meal) causes oxidative stress, chronic capillaries damage, acute endothelial damage, a rise in pro− tein glycation and adhesive molecules concentrations, and rise in blood clotting. These unfavorable processes lead to such diseases as type 2 diabetes, hypertension, and ischemic heart disease, and they are preceded by obesity. According to the findings of numerous studies, a low−GI diet contributes not only to lowering the amount of fatty tissue, but may also prevent metabolic diseases through its influence on blood glucose and lipoprotein concentra− tions. Due to the several advantages of a low−GI diet, it should be recommended especially to patients with dia− betes, dyslipidemia, as well as healthy people to prevent metabolic diseases. The presence of low−GI foods in the diet is supported by such organization as the World Health Organization (WHO), the American Diabetes Association (ADA), and the Canadian Diabetes Association (CDA) (Adv Clin Exp Med 2007, 16, 4, 577–588).

Key words:glycemic index, carbohydrates, metabolic diseases, diet.

Streszczenie

W latach 80. XX w. opracowano po raz pierwszy diety dla chorych na cukrzycę oparte na indeksie glikemicznym. Koncepcja indeksu glikemicznego (IG) porządkuje produkty spożywcze zawierające węglowodany w zależności od ich wpływu na stężenie glukozy po posiłku. Produkty o wysokim IG są to na ogół wysoko przetworzone i oczysz− czone produkty zawierające skrobię w postaci amylopektyny i cukry proste. Mogą zwiększać ryzyko chorób me− tabolicznych, wpływając na powstawanie oporności tkanek na insulinę. Dieta o małym IG poprawia wrażliwość komórek na insulinę. Stale utrzymujące się duże stężenie glukozy po posiłku (powyżej 140 mg/dl 2 godz. po po− siłku) powoduje przewlekłe uszkodzenie naczyń, ostre uszkodzenie śródbłonka, nasilenie glikacji białek, zwięk− szenie stężenia cząstek adhezyjnych oraz stresu oksydacyjnego i krzepliwości krwi. Wymienione niekorzystne pro− cesy toczące się w organizmie są przyczyną chorób cywilizacyjnych, takich jak: cukrzyca, nadciśnienie, niedo− krwienna choroba serca, których ujawnienie poprzedza otyłość. Wyniki badań świadczą o tym, że dieta o małych indeksach glikemicznych przyczynia się nie tylko do zmniejszenia nadmiernej ilości tkanki tłuszczowej, ale także, wpływając na stężenie glukozy i lipidów, może chronić przed rozwojem innych chorób metabolicznych. Korzyści płynące z diety niskoglikemicznej przemawiają za stosowaniem jej zwłaszcza u osób chorych na cukrzycę, z za− burzeniem stężenia lipidów lub u otyłych, a także u zdrowych w celu zapobiegania chorobom o podłożu metabo− licznym. Uwzględnienie w diecie produktów o małym indeksie i ładunku glikemicznym zalecają również takie organizacje jak: Światowa Organizacja Zdrowia, Amerykańskie Towarzystwo Diabetologiczne i Kanadyjskie To− warzystwo Diabetologiczne (Adv Clin Exp Med 2007, 16, 4, 577–588).

Nutrition plays a great role in the pathogenesis of overweight, obesity, and associated diseases such as hypertension, atherosclerosis, and type 2 diabetes mellitus. A special role in the etiology of these diseases is attributed to carbohydrates. Dietary carbohydrates, depending on their kind and amount, affect such metabolic parameters as the level of glucose and hormones which regulate its metabolism and of triglycerides. For many years discussions on the effect of carbohydrates on metabolic parameters have concentrated on their division into mono− and polysaccharides. The inclusion of products containing polysaccharides, such as starch, in the diet was advocated. Polysaccharides were not believed to cause a sud− den postprandial rise in blood glucose level. However, the opposite point of view was verified experimentally in the early 1980s and this resulted in the introduction of a new notion, the glycemic index (GI), which ranks foods according to their effect on postprandial glycemia [1]. The glycemic index is the quotient of the area above the glycemic curve obtained after consumption of a product containing 50 g of carbohydrates and the area below the glycemic curve obtained after the consumption of 50 g of glucose. The blood glu− cose level is assessed 0.5, 1, 1.5, and 2 hours after carbohydrate intake [2, 3]. The glycemic index was used to categorize all food products into three groups: those with low GI (recommended, below 55%), medium GI (allowed, 55–69%), and high GI (contraindicated, 70% and above).

In addition to the glycemic index, another important parameter is glycemic load (GL), which determines the content of absorbable carbohy− drates in the ingested food product. The glycemic load is the product of the food’s GI (%) and the amount of absorbable carbohydrates in the ingest− ed food mass (g) divided by 100 (%). Foods with low glycemic index usually have a low glycemic load. However, some foods, such as watermelon and broad beans, have a low glycemic load despite a high glycemic index due to the low amount of absorbable carbohydrates. The recommended daily glycemic load of the diet should not exceed 80 g, the allowable glycemic load ranges are from 80–120 g, and a daily glycemic load higher than 120 g is contraindicated and considered high [2].

What Determines

the Glycemic Index of a Food

The level of the glycemic response of the organism after the consumption of food is regulat− ed by numerous factors, among others by the kind and content of carbohydrates, the content of fiber,

protein, and fat, as well as by food processing [3]. It is assumed that the time of digestion and absorp− tion has a significant influence on postprandial changes in blood glucose levels. Fat in the food delays the hydrolysis and absorption of absorbable carbohydrates and in this way lowers the glycemic index of food. A similar role is played by protein. Gluten, the protein contained in bread and cereals (except cornflakes) forms a network around parti− cles of starch, hampering the access of hydrolyz− ing enzymes to carbohydrates. Lack of this protein is the reason for the increased glycemic index in gluten−free bread in comparison to bread contain− ing gluten [4]. Moreover, fiber in the food also decreases the GI as it delays gastric emptying and prolongs the time of digestion and absorption of consumed carbohydrates. However, a special role is attributed to the soluble fractions of fiber, espe− cially the pectin in fruit and vegetables, which, due to their viscosity, decrease the availability of starch to digestive enzymes [5]. A meal containing fruit and vegetables will have a lower glycemic index than the same meal without fruit and veg− etables.

The glycemic index of foods containing starch depends on the relation of amylose to amy− lopectin, the two chemical forms of starch in the food. Starchy products are bread, potatoes, groats, and pasta. The ideal situation is when most of the starch is in the form of amylase and amylopectin constitutes a minor portion. Amylose, due to its linear structure, forms a firm structure which is less susceptible to the action of digestive enzymes. It has a lower glycemic index than the easily hydrolyzed amylopectin, which has a branched chain. Changing the amylose−to−amylopectin ratio is often the reason for differences in the glycemic index of the same product, i.e. rice. The glycemic index of rice with high amylose content is 59%, while the variety with low amylase content has a GI of 88% [6].

Table 1.Glycemic index (GI) and glycemic load (GL) of selected food products (the glycemic index was calculated in relation to glucose) [8]

Tabela 1.Wartości indeksów (IG) i ładunków glikemicznych (ŁG) wybranych produktów (indeks glikemiczny dotyczący stężenia glukozy) [8]

GI GL

(IG) (ŁG)

% g

Low−GI foods Fruits:

(Produkty o niskim IG) (Owoce)

banana medium 120 g 52 12

(banan średni 120 g)

apple 120 g 38 6

(jabłko 120 g)

grapefruit 120 g 25 3

(grepfrut 120 g)

orange 120 g 42 4.6

(pomarańcza 120 g)

grapes, green 120 g 46 8

(winogrono zielone 120 g) Vegetables:

(Warzywa)

kidney beans, boiled 150 g 28 7

(fasola nerkowata, ugotowana 150 g)

dry beans boiled 150 g 29 9

(fasola suszona ugotowana 150 g)

frozen peas boiled 80 g 48 3

(groszek mrożony gotowany 80 g)

dry peas boiled 150 g 22 2

(groszek suszony gotowany 150 g)

carrot boiled 80 g 47 3

(marchew gotowana 80 g)

carrot raw 80 g 16 1

(marchew surowa 80 g) Beverages:

(Napoje)

apple juice 250 ml 40 11.7

(sok jabłkowy 250 ml)

orange juice 250 ml 50 4.6

(sok pomarańczowy 250 ml) Cereals:

(Produkty zbożowe)

pumpernickel rye bread 30 g 46 5.2

(chleb żytni Pumpernikiel 30 g)

buckwheat groats, boiled 150 g 54 30

(kasza gryczana gotowana 150 g)

barley groats boiled 150 g 25 11

(kasza jęczmienna gotowana 150 g)

rough pasta boiled 180 g 46 22

(makaron gruby gotowany 180 g)

brown rice boiled 150 g 55 17.9

(ryż brązowy gotowany 150 g)

white spaghetti boiled 180 g 44 21

(spaghetti białe gotowane 180 g) milk products:

(produkty mleczne)

full−fat milk 3.2% 250 ml 27 3

(mleko pełne 3,2% 250 ml)

sour milk 250 ml 11 1.3

(mleko zsiadłe 250 ml)

fruit yoghurt, skimmed 200 g 27 7

Table 1.Glycemic index (GI) and glycemic load (GL) of selected food products (the glycemic index was calculated in relation to glucose) [8] (cont.)

Tabela 1.Wartości indeksów (IG) i ładunków glikemicznych (ŁG) wybranych produktów (indeks glikemiczny dotyczący stężenia glukozy) [8] (cd)

GI GL

(IG) (ŁG)

% g

Low−GI foods Snacks:

(Produkty o niskim IG) (Przekąski)

sponge finger 60 g 46 15

(biszkopt 60 g)

milk chocolate 50 g 43 12

(czekolada mleczna 50 g)

bitter chocolate 50 g 22 6

(czekolada gorzka 50 g)

peanuts 50 g 14 1

(orzeszki ziemne 50 g) Foods with medium GI Cereals:

(Produkty o średnim IG) (Produkty zbożowe)

whole−meal rye bread 30 g 58 8

(chleb razowy żytni 30 g)

wheat grits 80 g 68 20

(kasza manna ugotowana 80 g)

pancakes 80 g 67 39

(naleśniki – ciasto 80 g)

muesli 30 g 66 17

(musli 30 g)

oatmeal 250 g 58 13

(płatki owsiane 250 g)

basmati rice boiled 150 g 58 22

(ryż basmati gotowany 150 g)

white rice boiled 150 g 64 23.3

(ryż biały gotowany 150 g)

brown rice boiled 150 g 55 18

(ryż brązowy gotowany 150 g) Beverages:

(Napoje)

coca Cola 250 ml 58 14.5

(coca cola 250 ml)

fanta 250 ml 68 23

(fanta 250 ml) Snacks: (Przekąski)

ice cream 50 g 61 8

(lody 50 g)

honey 25 g 55 10

(miód 25 g)

french croissants 57 g 67 17

(rogaliki francuskie 57 g) Fruit and vegetables: (Owoce I warzywa)

canned apricot in syrup 120 g 64 12

(morele z puszki w syropie 120 g)

raisins 60 g 64 28

(rodzynki 60 g)

beets 80 g 64 5

(buraki 80 g)

new potatoes boiled 150 g 57 12

(ziemniaki młode gotowane 150 g)

potatoes boiled 150 g 65 18

food in its most natural form, minimally pro− cessed, and cooked for the shortest possible time.

The glycemic index of a food is closely asso− ciated with the rate of digestion and absorption of the carbohydrates contained in it. The hydrolysis of foods with low GI occurs slowly and causes a mild elevation in the blood glucose level. Consumption of food with high GI results in fast digestion of carbohydrates and rapid elevation of blood glucose, which rises to high levels and then drops suddenly. This produces significant fluctua− tions in the levels of hormones such as insulin, glucagon, cortisol, adrenaline, and growth hor− mone, which regulate the metabolism of glucose and fatty acids. It was demonstrated that postpran−

dial hyperglycemia after the consumption of foods with high GI may lead to obesity, cardiovascular disease, and type 2 diabetes [9, 10].

The course of postprandial glycemia is closely associated with the glycemic index and glycemic load of the consumed food. Products with a low glycemic index, i.e. below 55%, include non− starchy vegetables, most fruits, pulses, nuts, pum− pernickel, coarse groats, durum pasta, as well as milk and milk products. Their consumption does not evoke sudden changes in blood glucose and insulin levels. On the other hand, the highest level of postprandial glycemia is observed after con− sumption of foods with high GI, i.e. above 70%. These include highly processed cereals, white

Table 1.Glycemic index (GI) and glycemic load (GL) of selected food products (the glycemic index was calculated in relation to glucose) [8] (cont.)

Tabela 1.Wartości indeksów (IG) i ładunków glikemicznych (ŁG) wybranych produktów (indeks glikemiczny dotyczący stężenia glukozy) [8] (cd.)

GI GL

(IG) (ŁG)

% g

Foods with high GI Fruit and vegetables: (Produkty o wysokim IG) (Owoce i warzywa)

watermelon 120 g 72 4

(arbuz 120 g)

broad beans 80 g 79 9

(bób 80 g)

potatoe French fries 150 g 75 22

(ziemniaki, frytki 150 g)

mashed boiled potatoes 150 g 74 15

(ziemniaki gotowane tłuczone 150 g)

baked potatoes 150 g 85 26

(ziemniaki pieczone 150 g) Cereals:

(Produkty zbożowe)

french baguette 30 g 95 15

(bagietka francuska 30 g)

white wheat bread 30 g 70 10

(chleb biały pszenny 30 g)

gluten−free bread 30 g 76 11

(chleb bezglutenowy 30 g)

millet groats cooked 150 g 71 25

(kasza jaglana gotowana 150 g)

wheat grits cooked 250 g 70 24.5

(kasza manna gotowana 250 g)

cornflakes 30 g 81 21

(płatki kukurydziane 30 g) Snacks:

(Przekąski)

vanilla wafers 25 g 77 14

(wafle waniliowe 25 g)

popcorn 20 g 72 8

(prażona kukurydza 20 g)

dry wafers 35 76 10

(wafle suche 35)

doughnuts 100 g 76 46

bread, cornflakes, fine and overcooked groats, vegetables with most of their starch in the form of amylopectin, e.g. mashed potatoes and French fries, and the majority of confectionery products. Table 1 lists the glycemic indexes and glycemic loads of selected products.

The Role of Hyperglycemia

in the Etiology

of Cardiovascular Disease

The consumption of foods with a high GI results in postprandial hyperglycemia and a de− crease in the level of antioxidants and, conse− quently, in oxidative stress [11]. Especially sus− ceptible to the effect of oxidative stress are endothelial cells, to which glucose diffuses regardless of insulin. The produced free radicals trigger the production of inflammatory cytokines and decrease the availability of nitrogen oxide, which plays a role in vasodilation [12]. The high insulin levels resulting from hyperglycemia stim− ulate the production of endothelin 1, a substance causing vascular contraction. This leads to impaired function of the endothelium and decreases vascular contractibility, consequently contributing to hypertension. Increased postpran− dial glycemia is responsible for dysfunction of the endothelium even in people with normal glucose tolerance [13].

Another negative effect of postprandial hyper− glycemia is the increased glycation of proteins. Advanced glycation end−products activate macro− phages and initiate a number of inflammatory reactions in endothelial cells. This leads to damage to the cells as a result of the increased permeabili− ty for lipoproteins as well as the adhesion and migration of leukocytes into the vascular wall. Damage to the endothelium initiates atherosclerot− ic processes. Hyperglycemia is also responsible for enhanced division of smooth muscle cells, which may foster the formation of atherosclerotic plaques [13].

An elevated glucose level exerts an unfavor− able effect on homeostasis by contributing to increased thrombocyte aggregation. Moreover, the formation of prostacycline, which exhibits anti− aggregative properties, is reduced as a result of endothelial damage. High levels of glucose impair fibrinolysis by increasing the synthesis of PAI−1 (plasminogen activator inhibitor). Hyperglycemia is thus responsible not only for the initiation of hypertension and atherosclerosis, but also for an increased risk of thrombotic incidents [13].

Glycemic Index

and Type 2 Diabetes

Mellitus and Obesity

A long−term diet with increased glycemic index leads to chronically elevated blood glucose and insulin levels. This condition leads to insulin resistance and limitations in the transport of glu− cose to the cells and its utilization as well as to increased levels of free fatty acids [9, 14, 15]. Long−term consumption of foods with high glycemic index may lead to overweight and obesi− ty as a result of the accumulation of adipose tissue stimulated by the action of insulin. Obese people show cellular resistance to insulin and increased levels of free fatty acids, from which fractions of atherogenic lipoproteins are synthesized in the liver [7]. Obesity is a metabolic disorder closely associ− ated with diabetes, cardiovascular disease, and hypertension, and for this reason the quality of con− sumed carbohydrates, expressed by their glycemic index, has a great significance both in the preven− tion and the control of these diseases. Central or abdominal obesity often accompanies impaired glucose and insulin metabolism, but also dyslipi− demia and hypertension. This disorder is referred to as “metabolic syndrome”. Metabolic syndrome has been increasingly diagnosed in a number of patients, and its etiopathogenetic factors include, among others, unhealthy eating habits. The risk of metabolic syndrome was estimated to be 40% lower in a group of people eating foods with the lowest GI [16]. This finding is associated with the beneficial effect of a low−glycemic diet on blood glucose and components of lipid metabolism.

the development of insulin resistance. A decrease in the level of free fatty acids improves glycemic control and sensitivity to insulin. Similar results were observed by Mc Keown et al. [16], who demonstrated a reduction in insulin resistance with a decrease in the glycemic index of the diet.

A diet rich in foods with low GI also contributes to the reduction of postprandial insulin level [10, 18]. Jenkins et al. [21] observed a 32% decrease in C−pep− tide level in the urine of patients keeping a medium− GI diet for two weeks compared with a group receiv− ing high−GI foods. C−peptide is formed during the conversion of proinsulin to insulin and the decrease in its level was a reflection of decreased insulin secre− tion in the subjects on a medium−GI diet.

Foods with a low GI not only decrease post− prandial levels of glucose and insulin, but also decrease the fasting level of glucose. Jimez−Cruz et al. [22] observed a significant reduction in glycemia in overweight patients and in patients with type 2 diabetes who were using a low−GI diet for six weeks. Percheron et al. [20] observed that the dis− turbances in carbohydrate metabolism in over− weight patients with impaired glucose tolerance increased significantly after consumption of foods with high GI. The patients demonstrated a signifi− cant increase in blood glucose level and a decreased rate of its intracellular metabolism after a high−GI meal in comparison with the group on a low−GI diet. A diet containing foods with low GI con− tributes to a remarkable, long−lasting improvement of glycemic control. Many authors [21–24] observed decreased levels of glycated proteins, such as glycated hemoglobin (HbA1c) and glycated albu−

min−fructosamine, the levels of which were directly proportional to the glycemic index of the diet [23].

Foods with low GI also contribute to an increase in the level of adiponectin, a cytokine secreted by adipocytes which increases the sensitiv− ity to insulin and exhibits a potential anti−athero− sclerotic effect [25]. Lower levels of adiponectin were observed in metabolically unbalanced dia− betes. A low−GI diet, by improving glycemic con− trol, may also play a significant role in modulating the adiponectin level. The level of this cytokine was shown to be 13% and 18% lower after consumption of foods with high glycemic index and load and 19% higher in subjects using a diet rich in fiber.

The Effect of Fiber

on Metabolic

Parameters of Blood

Foods rich in fiber have a protective effect against hyperglycemia and hyperinsulinemia

because they reduce postprandial blood glucose levels [9, 26]. Soluble fractions of fiber, especial− ly pectin, display a tendency to form a gel and may delay the absorption of glucose and thus lower the glycemic index of the meal. For this reason, foods rich in fiber, such as vegetables, fruit, and pulses, are especially recommended for patients with type 2 diabetes. A high fiber content in the diet also leads to increased sensitivity to insulin. Wolever et al. [27] compared glycemic and insulin response in subjects with hyperinsulinemia and with normal insulin levels after the consumption of cereals of various fiber content. Both groups showed lower postprandial glucose levels after the consumption of cereals rich in fiber; however, the level of insulin was lower only in the patients with hyper− insulinemia. Moreover, beneficial changes in lipid fraction levels and decreased body mass were observed in subjects eating whole−grain foods [26]. Overweight males showed an inverse rela− tionship between the content of fiber in food and physical activity and the blood levels of triglyc− erides and total cholesterol [28].

Due to the beneficial effect on lipid profile, eating foods rich in dietary fiber decreases the risk of cardiovascular disease. This role is attributed to the fractions of soluble fiber which, thanks to their viscosity, reduce the reverse absorption of bile acids in the alimentary tract and increase their excretion. This results in a decrease in cholesterol level and changes its metabolism to a pathways which foster the synthesis of bile acids. Subjects on a diet rich in soluble fiber also show an increased synthesis of deoxycholic acid, which inhibits HMG Co A (hydroxymethyl glutaryl coenzyme A reductase), an enzyme controlling the synthesis of endogenous cholesterol [29]. After the introduction of a diet rich in soluble fiber, patients with hyperlipidemia displayed favorable changes in the lipid profile, such as a decrease in the total cholesterol/HDL ratio and in apolipopro− tein B, a component of the LDL fraction, to A1 contained in the HDL ratio [30].

Glycemic Index of Diet

and Lipid Profile

addition, hyperinsulinemia, which is a response to elevated glycemia, enhances the cellular metabo− lism of glucose and stimulates lipogenesis. Insulin was shown to stimulate the activity of hydrox− ymethyl glutaryl coenzyme A reductase (HMG− CoA), an enzyme participating in the synthesis of endogenous cholesterol [32].

Especially exposed to hypertriglyceridemia are subjects with insulin resistance, who, due to decreased sensitivity to insulin, develop increased release of fatty acids from adipose tissue and their decreased passage to cells. The consequences include a high blood level of free fatty acids, which are converted to triglycerides in the liver. Moreover, insulin resistance is associated with increased activity of hepatic lipase, which fosters the formation of the LDL fraction. It was shown that an elevated level of these lipoproteins corre− lates negatively with the level of HDL cholesterol [33, 34]. Increased levels of triglycerides associat− ed with decreased sensitivity to insulin often occur in obese patients with metabolic syndrome [34]. It was observed that patients with insulin resistance and hyperglycemia and a body mass index (BMI) higher than 23 kg/m2_{are most exposed to cardio−}

vascular incidents [35].

In vitro studies demonstrated that a signifi− cantly elevated level of glucose increases the oxi− dation of cell membrane lipids, lipoproteins, pro− teins, and DNA, while in vivostudies revealed an increased level of reactive oxygen and decreased levels of antioxidants. These changes resulted in hypertension and fostered the formation of throm− bus [14]. A reduction in the level of HbA1c was

found to correlate with a decreased number of myocardial incidents in diabetic patients. On the other hand, a 1% rise in the level of HbA1cincreas−

es the risk of cardiovascular complications by about 25% [36].

Rizkalla et al. [18] demonstrated that a diet with low GI contributes to a significant reduction in the level of total cholesterol, its LDL fraction, and atherogenic apolipoprotein B. Moreover, they observed decreased activity of plasminogen acti− vator inhibitor (PAI−1), inhibiting the formation of plasmin, which plays a key role in the digestion of fibrin. Reduction in its activity was a positive prognostic factor in patients who had a tendency to form thrombus, and it also helped alleviate the risk of myocardial infarction and cerebral incident.

Heilbronn et al. [37] compared the effect of low−calorie diets with different GIs on glycemic control and lipid profile in overweight patients with diabetes. Both diets produced reductions in body mass and decreases in the levels of glycated hemoglobin, total cholesterol, LDL, and the total cholesterol/HDL ratio to a comparable extent.

Changes in the level of HbA1cand the lipid profile

were significant in patients on a low−GI diet. According to Kabir et al. [38], a decrease in the glycemic index from 60% to 40% in only one of the daily meals had a beneficial effect on the lipid profile in patients with type 2 diabetes. After four weeks of the diet, the studies revealed decreased levels of fasting cholesterol and apolipoprotein B as well as postprandial glycemia in patients eat− ing a breakfast with low GI [38].

An increase in the glycemic index and load of consumed foods results in elevated levels of triglycerides and a decreased level of HDL choles− terol [39, 40]. This association was especially sig− nificant in patients with BMI ≥ 25 kg/m2_{. Over−}

weight and obesity foster atherogenic changes in the blood vessels. Atherogenic vascular lesions result from the dyslipidemia and ongoing inflam− matory process induced by foods with high GI. A correlation has been observed between the level of C−reactive protein and increased glycemic index and load in the diet as well as the amount of consumed carbohydrates [41]. The level of C− reactive protein in overweight subjects was 1.6 mg/l for the lowest glycemic load and 5.0 mg/l for the highest, while in subjects of normal weight the level of C−reactive protein was 1.1 mg/l and 3.3 mg/l, respectively [41].

Body Mass Control

and Glycemic Iindex

of the Diet

in total cholesterol level by 13%, LDL cholesterol by 2%, triglycerides by 14%, and an increase in HDL cholesterol level by 17% [45].

The consumption of foods with high GI leads to the secretion of a large amount of insulin, an intensification of glucose conversion, and stimula− tion of lithogenesis, which is followed by a de− crease in the plasma levels of glucose and free fatty acids. Three to five hours after a meal the organism is deprived of the main sources of ener− gy. The more often hypoglycemia occurs, the more meals are consumed daily, which leads to over− weight and obesity [14]. Such violent changes in the level of glucose are not observed after foods with a low glycemic index. A slow decrease in the level of glucose and a reduction in hypoglycemia results in fewer meals during the day.

Prolonged hyperinsulinemia induced by foods with high glycemic index changes the metabolic pathway to one which fosters the growth of adi− pose tissue. Persons who had increased levels on insulin in their childhood are more predisposed to the growth of body mass [46]. Rats fed with high− GI carbohydrates revealed increased activity of fatty acids synthetase, enlarged adipocytes, and an increase in the expression of GLUT−4 gene, which codes a protein transporting glucose to the cell [47, 48]. Moreover, a diet based on foods with high GI leads to faster oxidation of glucose as induces the secretion of large amounts of insulin. Produced acetyl−CoA is converted to malonyl−CoA, which significantly inhibits the transport of fatty acids to the mitochondria and their oxidation [49]. In con− trast, eating foods with low GI helps avoid the negative effects of hyperinsulinemia and facili− tates the reduction of body mass by increasing satiety, resulting in a reduction in the number of daily meals [10, 49, 50]. The digestion and absorp− tion of foods with low GI occur less rapidly, which facilitates prolonged stimulation of the digestive tract receptors by enteroglucagon and cholecys− tokinin. Signals from these receptors reach the satiety center in the brain and cause its stimulation. This effect of a low−GI diet was confirmed by Ludvig et al. [10]. The participants of the trial received breakfast with the same caloric content but differing glycemic index for several consecu− tive days. The authors demonstrated that the inges− tion of foods with low GI was followed by a lower uptake of energy than after foods with medium and high GI. The difference was 53% and 83%, respectively. The subjects also reported higher satiety levels.

Reduction in the caloric content of foods is necessary to initiate the slimming process, and after some time it leads to physiological adaptive changes in the organism manifested by a decrease

in energy expenditure at rest [10, 51, 52]. These adaptive changes can be minimized by consuming foods with low GI [51]. It was shown that in over− weight subjects using a diet with low GI and lim− ited caloric content, the energy expenditure at rest decreased by 4.6%, but in patients on an isocaloric diet with high GI by 10.5%. Moreover, the sub− jects on the low−GI diet revealed lower postpran− dial levels of glucose and insulin, decreased appetite, and lowered levels of leptin, a hormone secreted by the adipose tissue responsible for sati− ety. The authors of the study suggest that the lower level of leptin may indicate increased sensitivity to satiety signals [52].

The glycemic index of the diet may also influ− ence the composition of body mass [48]. In a study conducted by Pawlak at al. [48] in which one group of rats received food with starch of high GI composed of 100% amylopectin and the other starch with lower GI containing 60% amylose and 20% amylopectin, the first group demonstrated highly accelerated growth of body mass accompa− nied by a significant increase in triglyceride levels and hyperinsulinemia. Moreover, the level of adi− pose tissue increased by 71% and fat−free body mass was reduced by 8% in comparison with the control group. Similar changes were observed in humans, in whom a reduction in adipose tissue, especially in the abdominal area, and a tendency to increase fat−free body mass were observed after five weeks of using foods with low GI in their diet [53].

The results of investigations [23, 40, 49, 52] prove that a low−GI diet contributes not only to a reduction in excessive amounts of adipose tissue, but also, through its effect on the level of glucose and lipids, may protect the organism against other metabolic disorders. The benefits of a low−GI diet prove the necessity of using it in patients with type 2 diabetes, dyslipidemia, obesity, as well as in healthy subjects to prevent diseases of metabolic origin.

The General Conditions

of Planning Meals

Containing Carbohydrate

Foods with Low Glycemic

Index and Load

minerals, their daily amount should not be lower than 130 g according to the American Diabetes Association [54]. A decrease in the GL in the diet should be accomplished first of all by changing the quality of ingested carbohydrates. When planning meals, one should first of all choose foods with low GI and limit the amount of and use smaller portions of foods with high GI. For this reason the diet should include large amounts of non−starchy vegetables, pulses, and fruit in the amount of 400–800 g daily. Foods containing white flour, such as white bread, confectionery, and potatoes, should by limited. They should be replaced by whole−meal bread, coarse groats, and pasta. It is important not to eat mashed and overcooked foods, as grinding, grating, and prolonged cooking time increase their GI.

As far as cereals are concerned, oatmeal and barley flakes are highly recommended, as they are a rich source of soluble fiber. It was observed that the fiber occurring naturally in cereals contributes to a decrease in the levels of glucose and insulin and improves the lipid profile. The effect of fiber on metabolic parameters is attributed to its feature of giving foods a specific structure which hampers its hydrolysis in the digestive tract. This effect has not been observed in guar gum, the soluble fiber used as a dietary supplement [55].

Apart from large amounts of non−starchy veg− etables and fruit, the diet should include low−fat milk products, oily sea fish, lean meat of land ani− mals, pulses, and nuts [50]. It is recommended to eliminate highly processed foods from the diet and to limit sweets and other products containing refined sugar.

Diets with Low Glycemic

Index and Load

and Dietary Guidelines

in Various Countries

The diets recommended in the European Union and in Poland [56, 57] (< 30% of the ener− gy source from fat, 14% from protein, and 56% from carbohydrates) do contribute to limiting the total and LDL cholesterol increase, but the high carbohydrate content, rising to 56% of the daily energy requirement, induces hypertriglyceridemia and leads to a decrease in HDL cholesterol level. The resultant changes in the lipid profile may lead to the production or exacerbation of atherogenic processes in the blood vessels. A diet with carbo− hydrate foods with low GI and GL is an alternative which is well documented scientifically. The con− cept of glycemic index categorizes foods contain− ing carbohydrates in relation to their effect on postprandial glycemia. Modifying a diet to lower its glycemic load may lead to a reduction in the amount of carbohydrates to about 40% of the ener− gy and to an increase in the participation of pro− teins as the source of energy to about 30%. Such proportions in the sources of energy from macro− components differ from the dietary guidelines in Poland. Despite the differences, the findings of many authors [21, 23, 38] confirm the beneficial effect of a low−GI diet on lipid profile and both postprandial and fasting glycemia. National and international health organizations, such as the WHO (World Health Organization) [3], the ADA (American Diabetes Association), and the CDA (Canadian Diabetology Association) [54], advo− cate the use of foods with low glycemic index and load in the diet; however, further studies evaluat− ing the remote effects of such a diet as well as its effect on the organism and functioning of internal organs are still required.

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Address for correspondence:

Bożena Regulska−Ilow

Department of Food Science and Nutrition Silesian Piasts University of Medicine pl. Nankiera 1

50−140 Wrocław Poland

Tel.: +48 71 784 02 09

E−mail: [email protected]

Conflict of interest: None declared