New Concepts in Diabetes and Its Treatment - part 3 docx

Dietary caloric restriction ameliorates hyperinsulinemia and mia in obese type 2 diabetics and improves other metabolic parameters; seetable 1 and reduces the incidence of type 2 diabete

muscles, adipose tissue and hepatocytes, while normalizing a wide range ofmetabolic abnormalities associated with insulin resistance Reported effectsinclude: (a) decrease in plasma triglyceride, FFA and LDL cholesterol levelsand increase in plasma HDL cholesterol; (b) increased expression of glucosetransporters GLUT-1 and GLUT-4; (c) activation of glycolysis in hepatocytes;(d) antagonism towards some of the effects of TNFa; (e) decrease in bloodpressure; (f ) inhibition of vascular smooth muscle cell proliferation andhypertrophy; (g) enhanced endothelium-dependent vasodilation, and (h) anti-oxidant action Finally, although thiazolidinediones do not stimulate insulinsecretion, they improve the secretory response ofb-cells to insulin secretagog-ues.

Rosiglitazone (a PPAR c Agonist) Rosiglitazone, like other

thiazolidine-dione compounds, is a PPARc agonist, inasmuch as it potently and specificallystimulates peroxisome proliferator-activated receptors-c (PPARc) and sensi-tizes cells to insulin Indeed, rosiglitazone is an antidiabetic agent which en-hances sensitivity to insulin in the liver, adipose tissue and muscle, resulting

in increased insulin-mediated glucose disposal This compound, therefore,improves insulin resistance, which is a key underlying metabolic abnormality

in most patients with type 2 diabetes In contrast with troglitazone, zone does not appear to be hepatotoxic, on the basis of clinical and in vitrostudies, and does not induce cytochrome P4503A4 metabolism However, thedrug is contraindicated in patients with history or signs/symptoms of liverdiseases and its use requires monitoring of liver function tests Moreover,rosiglitazone does not interact significantly with nifedipine, oral contraceptives,metformin, digoxin, ranitidine, or acarbose

rosiglita-In clinical trials, rosiglitazone 2–12 mg/day (as single daily dose or twodivided daily doses) improved glycemic control in type 2 diabetic patients, asshown by decrease in fasting plasma glucose and glycated hemoglobin(HbA1c) Addition of rosiglitazone 2–8 mg/day to existing sulfonylurea, met-formin or insulin therapy achieved reductions in fasting plasma glucose andHbA1c

Consistent with its mechanism of action, rosiglitazone appears to beassociated with a low risk of hypoglycemia (=2% of patients receiving mono-therapy) and did not increase the risk of alcohol-induced hypoglycemia

Other Compounds

The long-acting, nonsulfhydryl-containing ACE inhibitor, trandolapril,alone and in combination with the Ca2 +-channel blocker, verapamil, can sig-nificantly improve whole-body glucose metabolism by acting on the insulin-

sensitive skeletal muscle glucose transport system in obese Zucker rats Data

on the role of TNFa raise the possibility that pharmacological inhibition ofthis factor may provide a novel therapeutic target to treat patients with type 2diabetes

Suggested Reading

American Diabetes Association: Consensus Development Conference on Insulin Resistance, Nov 5–6,

1997 Diabetes Care 1998;21:310–314.

Bell PM, Hadden DR: Metformin Endocrinol Metab Clin North Am 1997;26:523–537.

Scheen AJ: Clinical pharmacokinetics of metformin Clin Pharmacokinet 1996;30:359–371.

Daniel JR, Hagmeyer KO: Metformin and insulin: Is there a role for combination therapy? Ann cother 1997;31:474–480.

Pharma-Davidson MB, Peters AL: An overview of metformin in the treatment of type 2 diabetes mellitus Am J Med 1997;102:99–110.

DeFronzo RA, Bonadonna RC, Ferrannini E: Pathogenesis of NIDDM: A balanced overview Diabetes Care 1992;15:318–368.

Melchior WR, Jaber LA: Metformin: An antihyperglycemic agent for treatment of type II diabetes Ann Pharmacother 1996;30:158–164.

UK Prospective Diabetes Study (UKPDS) Group: E ffect of intensive blood-glucose control with metformin

on complications in overweight patients with type 2 diabetes (UKPDS 34) Lancet 1998;352:854–865.

F Belfiore, Institute of Internal Medicine, University of Catania, Ospedale Garibaldi,

I–95123 Catania (Italy)

Tel +39 095 330981, Fax +39 095 310899, E-Mail francesco.belfiore@iol.it

Dietary caloric restriction ameliorates hyperinsulinemia and mia in obese type 2 diabetics (and improves other metabolic parameters; seetable 1) and reduces the incidence of type 2 diabetes in subjects at risk or withimpaired glucose tolerance (IGT) Glucose tolerance and insulin sensitivityimprove when normal body weight is achieved or approached Indeed, even

hyperglyce-a 7–10% of weight loss is enough to improve insulin resisthyperglyce-ance in hyperglyce-all obesetype 2 diabetics Nutritional needs are different in type 1 (lean) or type 2(overweight or obese) diabetic patients Diet education is crucial and requiresthe participation of the patient and its family in the planning-diet process and

in the implementation of the adequate strategies to promote adherence todietary intervention

Goals of dietary therapy in diabetes are to reach and maintain ideal bodyweight (IBW), to maintain fasting and postprandial glycemic levels as close

as possible to normal and to achieve optimal blood lipid values, while providingadequate caloric intake as required for the various metabolic needs

Table 1 Effects of weight loss on altered

parameters in obese type 2 diabetics Insulin resistanceB

Hyperglycemia B Hypertriglyceridemia B Total hypercholesterolemia B LDL cholesterol B HDL cholesterol C Hypertension B

Modern recommended diet for diabetes is relatively high in complex hydrates (55–60% of total calories) and fibers, low in fats (25–30%) especiallysaturated (=10%, to reduce dyslipidemia and atherosclerosis associated todiabetes) and limited, but adequate, in proteins (15%)

carbo-Body Weight and Fat Distribution

Increase in body weight (related to height) or frank obesity are highlyrelevant to the pathogenesis of type 2 diabetes The ‘ideal’ body weight (actuallythe weight associated with the lowest mortality) for each inch of height can

be derived from the 1983 Metropolitan Life Insurance Weights for Heightstables, referring to 4.2 million subjects aged 20–59 For people over 55, thetables of median weights derived from the data of the National Health andNutrition Examination Surveys (NHANES) may also be used A commonlyused parameter relating weight to height is the body mass index (BMI), which

is calculated as follows: BMI>weight (kg)/height (m)2 In the clinical setting,

a BMI from 20 to 25 can be regarded as ‘normal’ while a BMI?27 can beregarded as indicative of overweight In some studies, the following valueshave been suggested for the BMI:=23.9>normal value for women; =25>normal value for men; 23.9–28.6 (female) and 25–30 (male)>overweight;

?28.6 (female) or ?30 (male)>obesity In 1995, the WHO established thefollowing BMI values: normal>18.5–24.9; overweight, 1st degree>25.0–29.9;overweight, 2nd degree (or obesity)>30.0–39.9; overweight, 3rd degree (orsevere obesity) q40 It should be noted that the BMI associated with thelowest mortality increases with age, ranging from=20 at age 20 to about 28

at age 70

It should be noted that from the above values of BMI it is possible

to calculate the corresponding weight values through the formula: weight(kg)>BMI¶height (m)2

Assessment of adipose tissue distribution is of mount importance to distinguish between visceral (or central or abdominal

para-or android) obesity and subcutaneous (para-or gynoid) obesity A largely usedparameter is the the waist-to-hip ratio (WHR), i.e the ratio between thecircumference at the waist and that at hip level The cut-off value distin-guishing normal from abnormal WHR has not yet been definitely established.

In some studies, values of WHR ?0.81 for female and ?0.92 for malesubjects were considered indicative of visceral/android obesity whereas lowerWHR values were regarded as indicative of subcutaneous/gynoid obesity.The American Heart Association has reported that a WHR ?0.80 should

be used to indicate increased risk of cardiovascular disease in women Otherrecent data suggest an upward shift in the critical threshold for WHR toq0.90, at which point there is an elevation in cardiovascular disease riskfactors

It has also been shown that the simple waist circumference is a goodindex of central (visceral) obesity, as is also the sagittal diameter The values

of waist circumference indicating increased visceral fat and cardiovascular riskwere found to be ?94 cm in men and ?80 cm in women Recently, it hasbeen reported that, while a waist circumferenceq96.5 cm is associated withhigh cardiovascular risk, even a waist circumferenceq76.2 cm entails signifi-cant risk Interestingly, threshold values of waist girth corresponding to criticalamounts of visceral adipose tissue do not appear to be influenced by sex or

by the degree of obesity It has also been estimated that a waist girth ofapproximately 95 cm in both sexes, WHR values of 0.94 in men and of 0.88

in women, and sagittal diameters of 22.8 cm in men and 25.2 cm in womencorrespond to a critical amount of visceral adipose tissue, equal to a fat area

of 130 cm2

The amount of intra-abdominal (visceral) fat may be preciselymeasured with computed tomography (CT), which however is an expensiveprocedure Echography is also being used to quantify the fat tissue and itsdistribution

Total Caloric Requirement

The caloric requirement of diabetic patients is similar to that of normalsubjects and changes with age, sex and occupational daily work or physicalactivity (i.e patients engaged in a heavy activity require a larger caloric intake).Other factors may influence dietary regimen, as the type of diabetes andthe associated diseases In lean adult diabetic patients, caloric intake shouldmaintain a normal weight, while in obese diabetic patients (especially withupper body fat distribution) a caloric restriction is required to achieve adesirable weight Noticeably, dietary restriction may improve metabolic controleven before weight loss is attained

Sedentary normal patients need approximately 30 cal/kg IBW/day whileactive normal patients need approximately 35–40 cal/kg/day Overweight sed-entary patients need 20–25 cal/kg/day and active obese patients need 30–35cal/kg/day, while underweight patients need 35 cal/kg/day if sedentary and40–50 cal/kg/day if active In elderly sedentary diabetic patients, 20 cal/kg/dayare usually required (after 50 years of age approximately 10% less calories foreach decade is required).

A more accurate assessment of the caloric needs may be achieved by usingappropriate formulas to calculate the rest metabolic rate (RMR), such as those

of Harris & Benedict which are based on weight, height, age and sex Sincesubjects of the same weight but of different height have similar RMR, formulasmay be simplified by considering only weight, age and sex RMR should beincreased by 30, 50 or 70% for low, medium or high levels of physical activity.Table 2 shows the caloric requirement according sex and age for selectedweights and activity levels, based on similar formulas

In diabetic children the caloric needs depend on the rate of growth andactivity pattern Children 4–6 years old require 90 cal/kg/day and children7–10 years old require 80 cal/kg/day It is important to allow an adequatecaloric intake in juvenile diabetes Caloric requirement in children may also

be calculated by adding to the baseline value of 1,000 cal/day the amount of100–125 cal for every year of age up to 12 years Youngsters should consume

3 meals daily with 2 or 3 snacks (eaten at the same time each day) to minimizeglycemic fluctuations and the risk of hypoglycemic episodes After the caloriccontent and the composition of the diet are established, the prescription of adiet was in the past made by utilizing the data in the Exchange Lists for MealPlanning published by the American Diabetes Association A more usefulapproach might be to use the precalculated diets (of various caloric content)prepared by several diabetes associations or other authoritative sources How-ever, it is now recognized that the diet should be individualized and prepared

by taking into account the eating habits and other lifestyle factors

It is clinically relevant that 7–35% of adolescent females with type 1diabetes may have an eating disorder, such as anorexia or bulima nervosa

Dietary Components

Dietary Carbohydrate

Carbohydrates are the most important source of energy and provide about

4 cal/g The carbohydrate intake of diabetic patients should be equal to that

of nondiabetic subjects A dietary carbohydrate content of about 50–60% oftotal energy intake seems adequate in diabetic patients

Table 2 Caloric needs according to age, sex, weight and physical activity

Sex and Weight Physical activity

kcal/kg kcal/day kcal/kg kcal/day kcal/kg kcal/day kcal/kg kcal/day

for 18- to 30-year-old men: (0.0630 ¶kg weight+2.8957)¶240;

for 31- to 60-year-old men: (0.0484 ¶kg weight+3.6534)¶240;

for 18- to 30-year-old women: (0.0621 ¶kg weight+2.0357)¶240;

for 31- to 60-year-old women: (0.0342 ¶kg weight+3.5377)¶240.

RMR was then multiplied by 1.3, 1.5 or 1.7 for low, medium or high physical activity, respectively.

Carbohydrates are available as complex or simple sugars In diabeticpatients, complex carbohydrates or polysaccharides should be preferred Com-plex carbohydrates include: starches (present in large amounts in rice, cereals,potatoes, pulses and vegetable roots), dextrins (derived from hydrolyzedstarch), glycogen (contained in liver and muscle), cellulose or pectins (indigest-

Table 3 Glycemic index of some foods

in beetroot and sugar cane, lactose present in milk, and maltose derivedfrom hydrolyzed starch) The formerly claimed diabetogenic effect of sucroseoverconsumption has not been confirmed by epidemiological or experimentalstudies However, in diabetic patients, sucrose-rich foods cause a rapid rise inglycemic values, which can be prevented by consuming these foods as part of

a mixed meal The recommended disaccharide (sucrose plus other containing disaccharides) consumption by diabetic people should not exceed5–10% of the total caloric intake Sucrose addition as sweetener should notexceed 20 g/day Fructose is a natural monosaccharide, used as a sweetener

glucose-It is converted to glucose (and stored as glycogen) or triglyceride in liver

In diabetics with insulin deficiency and impaired hepatic glycogen synthesis,fructose-derived glucose contributes to the hyperglycemia Thus, the safety offructose use in diabetes is a debated topic Starches are hydrolyzed to dextrins,then to maltose and finally to glucose (through the effect of gastric acid andintestinal enzymes) They are useful in the diabetic diet because they areslowly digested and absorbed, inducing lower increments of the glycemic andinsulinemic values than equivalent amounts of glucose or simple sugars

It is well established that equimolar amounts of carbohydrate in differentfoods induce different glycemic postprandial excursions Jenkins et al [1981]have elaborated a ‘glycemic index’, representing the incremental area under

2 h glycemic curve of food divided by the corresponding area under 2 hglycemic curve after ingestion of a portion of white bread containing equivalentamounts of carbohydrates, multiplied by 100 (table 3) Reference can also bemade to the glycemic response after glucose ingestion, in which instance theglycemic index for glucose is 100 Foods containing simple sugars have a highglycemic index, raising glycemia and insulinemia faster and to a greater extent,and therefore are contraindicated in diabetic patients However, several factorscan influence the food glycemic response, including: (a) type of diabetes, age,

sex, body weight, physical activity and race; (b) physical form of starches, size

of food particles, food processing and preparation, fiber or fat or proteincontent of food, different digestion or absorption or transit of different starch-

or sugar-containing foods, etc

Dietary Fat

Fats are an important source of energy, providing about 9 cal/g, and

difference in the amount and type of dietary fat can have relevant metabolic

effects In patients with IGT or type 2 diabetes or decompensated type 1diabetes, elevated plasma levels of triglycerides and cholesterol frequentlyoccur Both hypertriglyceridemia and hypercholesterolemia respond in part

to diet alterations The recommended fat intake is p30% of total calories(=10% of saturated fats, 6–8% of polyunsaturated fats and 14–12% of mono-unsaturated fats given as olive oil) Low-fat diets are often high in carbohy-drate (being the proportion of proteins relatively constant), which may favorhypertriglyceridemia This effect may be attenuated by supplementation withfibers

Saturated fats (which are solid at room temperature) are most often fromanimal source (milk, butter, cheese, bacon fat, fatty meat, etc.), but they arealso contained in high concentrations in coconut and palm oils Diets high insaturated fat are atherogenic (increasing total and LDL cholesterol levels) andfavor insulin resistance; thus, a diet restricted in saturated fats is recommended.Unsaturated fats (which are liquid at room temperature) derive from vegetablesource and include monounsaturated and polyunsaturated fats A diet high

in monounsaturated fatty acids or MUFA (most often assumed as olive oil,

as it occurs with the Mediterranean diet) does not increase LDL levels, mayimprove insulin sensitivity, glycemic control and HDL cholesterol levels, anddecreases plasma triglycerides For this reason, the American Diabetes Associ-ation (ADA) and the European Association for the Study of Diabetes (EASD)set free the intake of monounsaturated fat in diabetic patients On the contrary,

a diet high in polyunsaturated fatty acids or PUFA (such as corn, sunflowerand safflower oils) reduces total and LDL cholesterol but decreases HDLcholesterol as well; moreover, some data from the literature would suggestthat they may promote carcinogenesis in experimental animals

The intake of cholesterol should be restricted to=300 mg daily, avoidingcholesterol-rich foods (table 4), which can produce a 15–20% reduction ofplasma cholesterol level Excessive cholesterol intake causes increase in totalplasma cholesterol and LDL cholesterol, which can be reduced by increasingthe polyunsaturated/saturated fat ratio (which should be kept at?0.8).The polyunsaturated fatty acids of the omega-3 class (eicosapentaenoicand docosahexaenoic acids), which can be formed from a-linolenic acid

Table 4 Cholesterol content of some foods (mg/100 g)

Chicken liver 746 Cheese, cheddar 100

(through elongation and desaturation), are contained in fish oils and are useful

to reduce the coronary risk of diabetic patients (decreasing VLDL production,lowering arterial blood pressure, reducing platelet aggregation and prolongingbleeding time) This explains the low prevalence of coronary heart disease inthe Greenland Eskimos (consuming 5–10 g of fish oil fatty acids daily for alifetime) and in the Japanese fish eaters of coastal villages A dietary supplemen-tation with fish or fish oil should, therefore, be recommended It would beadvisable to replace in 2–3 meals a week the red meat with fish However, threeconsiderations speak against an excessive intake of fish or fish oil: (a) fishes ofcoastal waters and lakes accumulate a large quantity of mercury and chlori-nated hydrocarbons; (b) in some type 2 diabetic patients, 3-omega fatty acidsmay deteriorate glycemia (both increasing hepatic glucose production andimpairing insulin secretion), and (c) in patients with hypercholesterolemia butwithout hypertriglyceridemia the metabolic effects of fish oil are uncertain.Recently, new fat substitutes were proposed for use in the diet of diabeticpatients One of these products is named Olestra and is made from sucroseand long-chain fatty acids, is heat-stable, tastes like vegetable oil, promotescholesterol excretion and is calorie-free being not metabolized or absorbed.Another fat substitute is named Simpless and is made from egg white or wheyprotein of milk (using a process of microparticulation which confers a taste

of fat), has a low-calorie content, and is useful to make ice-cream, yogurt,margarine, cheeses, etc

Dietary Protein

Proteins are formed by amino acids and provide about 4 cal/g of energy.Some amino acids cannot be synthesized by humans and must be introducedwith diet (essential amino acids) The animal proteins (contained in meat,chicken, fish, egg, milk, etc.) are of high biological value, containing adequateamount of essential amino acids, while vegetable proteins (peas, beans, dryfruits, cereals, etc.) are of low biological value, laking some essential aminoacids Leucine and arginine have important biologic effects, stimulating insulin

secretion, while other amino acids are gluconeogenic and ketogenic Theamount of proteins that should be recommended to diabetic patients dependsupon several factors, such as the patient age, the nutritional status (undernutri-tion or malnutrition) and particular situations (growing, pregnancy, lactation,debilitating diseases, nephropathy, uremia, hepatic diseases, etc.).

The role of dietary protein in the development and progression of diabeticnephropathy is debated while it is clearly defined that a moderately low proteindiet is the best approach for treating renal disease of diabetic patients (seechapter on Diabetic Nephropathy) The recommended amount of proteins indiabetic diet is of 12–20% of total calories In diabetic subjects a high-proteindiet can increase renal blood flow, glomerular filtration rate and intra-glomerular pressure, accelerating glomerulosclerosis to end-stage renal failure(Brenner’s hypothesis) It is useful to substitute, at least in part, vegetableproteins for animal proteins, even if proteins from animal source do not seem

to significantly increase kidney workload In subclinical or incipient stages ofdiabetic nephropathy, glycemic control and low protein intake (0.8 g/kg IBW/day) may reduce renal blood flow, restore normal glomerular hemodynamics,decrease proteinuria and delay the progression of nephropathy In overt diabeticnephropathy with albumin excretion, the recommended protein restrictionshould be from 0.6 to 0.8 g/kg/day In cases of protein restriction, essentialamino acids should be supplemented To maintain energy balance, a lowprotein diet must be high in carbohydrates and fats and may exacerbatehyperglycemia, hypertriglyceridemia or hyperinsulinemia, increasing total andLDL cholesterol and decreasing HDL cholesterol Moreover, in diabetic pa-tients a low protein dietary content may favor a negative nitrogen balance andmuscle wasting

Dietary Fibers

In normal subjects and type 2 diabetic patients, several studies strated an improvement of glucose tolerance and a reduction of insulin secre-tion when a diet high in fiber was consumed In type 1 diabetics, high-fiberdiet was found to decrease glycosuria, as well as basal and postprandialglycemic levels Moreover, high-fıber intake may improve other metabolicparameters, and may also exert a preventive effect on cancer of bowel anddiverticular disease (diseases favored by the modern tendency to consume low-fiber, refined foods) Dietary fibers are heterogeneous and consist of severalcomplex polysaccharides resistant to gastrointestinal digestive enzymes (even

demon-if certain fibers are metabolized in the colon) Fibers can be water soluble orinsoluble and their effects are variable according to the different biochemical-physiological characteristics Celluloses, hemicelluloses and lignins bind waterand cations and are insoluble (wheat products and bran) whereas pectins,

Table 5 Foods naturally rich in fibers

Legumes Beans, peas, chickpeas, lentils

Vegetables Broccoli, artichokes, zucchini, carrots, eggplants, string beans, squash, potatoes,

tomatoes, celery, cabbage, onions, beets, fennels, turnips, radishes, asparagus, cucumbers, cauliflower, mushrooms

Fruits Apples, blackberries, pears, strawberries, oranges, plums, bananas, grapefruit,

pineapples, peaches, cherries, apricots, kiwis, mandarins

Cereals Bran (100%), bread (rye), bread (whole-grain wheat), rice, wheat flour (whole

grain)

gums and mucilages form gels and are soluble (oats, fruits and legumes) Thefoods naturally rich in fibers are legumes, roots, tubers, whole-grain cereals,fruits and green leafy vegetables (table 5)

Usually, the soluble fibers (especially those with high viscosity) exert usefulmetabolic effects, whereas insoluble fibers contribute to increase fecal bulk,promote movements of intestinal content, being useful in constipation (whichmay also result from autonomic diabetic neuropathy) The physiological effects

of fibers are influenced by osmolality or pH, mixture of fibers and foods,water retention, fermentation by bacteria, etc Soluble fibers would exert theirbeneficial effects on carbohydrate and lipid metabolism through several mecha-nisms, which include: (a) satiating effect; (b) delayed gastric emptying time;(c) decreased release of gut hormones, including intestinal insulin secretagogues(as GIP); (d) delayed small intestine transit time and altered colonic emptyingtime; (e) binding of bile acids, with impaired intestinal absorption of choles-terol; (f ) formation of gels that sequester or hide nutrients (carbohydrates,fats, cholesterol, etc.), providing a physical barrier that separates complexcarbohydrates from digestive enzymes, with reduced digestion and absorption

in small intestine; (g) increase of fecal bulk with accelerated intestinal transit,which may reduce absorption of nutrients; (h) fermentation by the bacteria

in the colon to gases and short-chain fatty acids, which would suppress cogenesis, and (i) improved peripheral insulin sensitivity and increased insulinreceptor binding

neoglu-It is interesting that fibers have the best effects when naturally contained

in aliments while they have poorer effects when added as pharmaceuticalproducts to dietary foods Diets useful to improve both fasting and postpran-dial hyperglycemia in diabetic patients have been suggested, which are rich

in fibers naturally contained in foods These diets are very rich in drates (up to 70%) and fibers (up to 35 g/day/1,000 kcal, both in soluble

carbohy-and insoluble forms) In these fiber-rich diets, fibers would mitigate thedeleterious effect of the high carbohydrate content on glucose metabolism,and would reduce total or LDL cholesterol and triglycerides (only in dia-betics), while lowering blood pressure and favoring weight loss in obesepatients In hypocaloric diets, the usually recommended fiber supplementation

is in the amount of 25 g/1,000 kcal (associated with high water assumption

to induce fiber swelling)

High-fiber diets can cause (especially in the first 7–10 days) cramping,abdominal discomfort, flatulence and diarrhea These diets may also impairabsorption of minerals and vitamins if used for a long time (in which instance,supplementation of calcium, trace elements and vitamins may be required).They may also increase the risk of bezoar formation, especially when a diethigh in fibers is contraindicated (patients with gastrointestinal dysfunction,gastroparesis or altered absorption from pancreatic enzyme deficiency) Largeamounts of dietary fibers may not be well tolerated by children, pregnantdiabetic women and elderly subjects

Alcohol and Other Nutrients

Alcohol provides about 7 cal/g, is not a food but is another source ofenergy that should be considered in a dietary plan Interestingly, in women adecreased risk (50%) of developing diabetes with increasing alcohol intakewas found and this effect was probably related to lower BMI linked withalcohol consumption Allowed intake should not exceed 10 g/day Excessivealcohol intake should be avoided in diabetic patients, because it inhibits glu-coneogenesis and can favor hypoglycemic episodes in subjects treated withinsulin or drugs In hypertriglyceridemic patients, alcohol may exacerbatedyslipidemia and liver steatosis

Diabetic patients may also suffer from associated diseases which requirespecial modified diets In the presence of congestive heart failure, hypertensionand kidney disease, dietary sodium should be restricted The sodium restrictionmay range from 500 to 1,000 mg/day (maximum intake=3 g/day), althoughthe use of diuretics may reduce the need for a severe sodium restriction,which makes foods less palatable and may provocate hypotension and fluid

or electrolyte disorders

Sweeteners

Sweeteners can be distinguished into caloric (or natural) sweeteners andnoncaloric (or artificial) sweeteners (table 6) In both type 1 and 2 diabeticpatients, the classical sweetener, sucrose, can be allowed in the maximumamount of 20 g/day, especially if associated to a mixed meal, because it does notdeteriorate metabolic control An excessive sucrose intake should be avoided,