Diabetes mellitus is a metabolic disorder characterized by high blood glucose levels and defective carbohydrate utilization due to a relative or absolute deficiency of insulin. As described in Chapter 5, there are two distinct primary forms of diabetes mellitus: type I, or insulin-dependent diabetes mellitus (IDDM), and type II, or noninsulin-dependent diabetes mellitus (NIDDM). This classification replaces the older terminologyjuvenile-onset and adult-onset diabetes. IDDM usually results from destruction of the insulin-secreting beta cells in the pancreatic islets of Langerhans. It is believed to be linked to the immune system, i.e., there is an increased risk of IDDM in subjects with certain genes associated with the histocompatibility immune response (HLA) genes. In the United States, approximately 5 to 10% of the people with diabetes have IDDM. NIDDM is much more common; it is associated with unknown genetic factors and aging and is closely linked to the insulin resistance associated with adiposity (see Chapter 21). The very high concordance of the incidence of NIDDM in many identical twin pairs (Barnett et al., 1981) suggests that genes play a very important role in this disease. Little is known about gene-environment interactions in the etiology of NIDDM.
Diabetes (IDDM and NIDDM) is diagnosed by the presence of classical symptoms and elevated glucose levels (Callaway and Rossini, 1987). The disease has been diagnosed in approximately 6 million people in the United States, and an additional 4 million to 5 million individuals are believed to have undiagnosed diabetes (National Diabetes Data Group, 1985). Each year, approximately 500,000 new cases are diagnosed. IDDM afflicts about 0.3% of the population after age 20. NIDDM has been diagnosed in approximately 2.4% of the total population; among those 65 and older, almost 9% of the population may have this disease (Callaway and Rossini, 1987).
In the general U.S. population, more women than men are afflicted with diabetes (both IDDM and NIDDM). However, when corrections are made for degree of adiposity in men and women, the prevalence of the disease is greater among men. This may be attributable to the regional distribution of fat, which is strongly determined by genetic factors (see Chapter 4).
Interpopulation variations in the prevalence of diabetes are large and frequently attributable to environmental differences. In general, the intercountry incidence rates are correlated to the level of socioeconomic development. For example, rates in Central American and Southeast Asian countries are generally lower than those in Westernized countries.
There is an increased incidence of NIDDM with increasing age. Within age groups, demographic characteristics of diabetics are very similar to those of the general U.S. population. These character-
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Page 627 24 Diabetes Mellitus Diabetes mellitus is a metabolic disorder characterized by high blood glucose levels and defective carbohydrate utilization due to a relative or absolute deficiency of insulin. As described in Chapter 5, there are two distinct primary forms of diabetes mellitus: type I, or insulin-dependent diabetes mellitus (IDDM), and type II, or noninsulin-dependent diabetes mellitus (NIDDM). This classification replaces the older terminologyjuvenile-onset and adult-onset diabetes. IDDM usually results from destruction of the insulin-secreting beta cells in the pancreatic islets of Langerhans. It is believed to be linked to the immune system, i.e., there is an increased risk of IDDM in subjects with certain genes associated with the histocompatibility immune response (HLA) genes. In the United States, approximately 5 to 10% of the people with diabetes have IDDM. NIDDM is much more common; it is associated with unknown genetic factors and aging and is closely linked to the insulin resistance associated with adiposity (see Chapter 21). The very high concordance of the incidence of NIDDM in many identical twin pairs (Barnett et al., 1981) suggests that genes play a very important role in this disease. Little is known about gene-environment interactions in the etiology of NIDDM. Diabetes (IDDM and NIDDM) is diagnosed by the presence of classical symptoms and elevated glucose levels (Callaway and Rossini, 1987). The disease has been diagnosed in approximately 6 million people in the United States, and an additional 4 million to 5 million individuals are believed to have undiagnosed diabetes (National Diabetes Data Group, 1985). Each year, approximately 500,000 new cases are diagnosed. IDDM afflicts about 0.3% of the population after age 20. NIDDM has been diagnosed in approximately 2.4% of the total population; among those 65 and older, almost 9% of the population may have this disease (Callaway and Rossini, 1987). In the general U.S. population, more women than men are afflicted with diabetes (both IDDM and NIDDM). However, when corrections are made for degree of adiposity in men and women, the prevalence of the disease is greater among men. This may be attributable to the regional distribution of fat, which is strongly determined by genetic factors (see Chapter 4). Interpopulation variations in the prevalence of diabetes are large and frequently attributable to environmental differences. In general, the intercountry incidence rates are correlated to the level of socioeconomic development. For example, rates in Central American and Southeast Asian countries are generally lower than those in Westernized countries. There is an increased incidence of NIDDM with increasing age. Within age groups, demographic characteristics of diabetics are very similar to those of the general U.S. population. These character-
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Page 628 istics include region and location of residence, marital status, and living arrangements. However, people with NIDDM have fewer years of schooling, are less likely to be employed, and have lower family incomes than the general adult population. Rates of NIDDM in the United States tend to be higher in rural areas and among people with relatively low socioeconomic status. Genetic, environmental, and lifestyle factors can place a person at increased risk for developing NIDDM. Rates of NIDDM among adults of Hispanic origin, blacks, and Asian-Americans appear to be higher than among whites. The rates of diagnosed NIDDM among some Native Americans (e.g., Pima Indians) are among the highest in the world. It is likely, however, that this high frequency reflects a genetic origin. The most important risk factors for NIDDM are increasing age, higher blood glucose concentration, family history of diabetes, and adiposity. Central distribution of body fat (i.e., high waist-to-hip ratio) is also strongly associated with a higher risk of NIDDM (see Chapters 5 and 21). Advanced maternal age and the presence of islet cell or insulin antibodies are associated with increased IDDM risk. The incidence of IDDM is similar in males and females, but is 1.5 times higher in whites than in blacks. Although incidence rates vary widely internationally, the risk for siblings of IDDM cases is 7 to 18 times higher than the risk in the general population. Siblings with certain HLA genes are at increased risk for developing IDDM (National Diabetes Data Group, 1985). Evidence Associating Dietary Factors with Diabetes Mellitus Epidemiologic and Clinical Studies The only factor that has been consistently related to the prevalence of diabetes mellitus is relative body weight (West, 1978). In several migrant populations (e.g., Japanese who moved to Hawaii and California and Yemenites who migrated to Israel), the prevalence of diabetes has increased along with Westernization of diet and lifestyle (West, 1978). The association of diabetes (presumably NIDDM) with adiposity persists in both inter- and intrapopulation analyses, despite wide variation in intake of individual nutrients. The prevalence of diabetes among adults is positively associated with higher percentages of total caloric intake as fats and inversely related to the percentage of calories as carbohydrates. Specific carbohydrates, such as sugar or starch, have not been shown to influence the risk of diabetes. In a study comparing two Micronesian populationsone at high risk and one at low risk of NIDDMKing et al. (1984) found that estimates of fiber intake had no predictive value in estimating risk of subsequent disease. Metabolic studies indicate that soluble forms of dietary fiber (e.g., guar and pectin) may curtail the glycemic response (glucose levels reached in response to ingestion of a particular food) in people with overt diabetes (Jenkins et al., 1976, 1978, 1979; Monnier et al., 1978; Morgan et al., 1979; LSRO, 1987; Poynard et al., 1980), but there are no data on the possible role of dietary fiber in reducing the risk for this disease. In large population studies, alcohol intake has been correlated with hyperglycemia. There is no ready explanation for this, except for alcoholics who develop insulin deficiency as a result of chronic pancreatitis. It was suspected that ethanol per se impaired glucose tolerance (Gerard et al., 1977). Yki-Järvinen and Nikkilä (1985) reported that insulin resistance results from excessive alcohol intake by otherwise healthy adults in the United States. Studies in animals indicate that a decrease in glucose tolerance is induced by chromium deficiency and is reversed by the administration of chromium (see Chapter 14). In hyperglycemic humans, chromium supplementation improved glucose tolerance and lowered insulin levels (Anderson, 1986; Riales and Albrink, 1981; Simonoff, 1984), suggesting that chromium deficiency may be a contributing factor to disease onset. However, no population data have been reported implicating chromium deficiency in humans with diabetes, and chromium supplementation does not improve blood glucose or insulin levels in those with the disease (Anderson, 1986; Rabinowitz et al., 1983). Chromium deficiency in people with diabetes could thus be a consequence rather than a cause of the disease (Simonoff, 1984). In summary, other than data on total caloric intake and NIDDM, there is no evidence that dietary composition influences the risk of diabetes mellitus. There is a long-standing controversy concerning the macronutrient composition of the diet used for management of people with IDDM and NIDDM (Bierman, 1979; Wood and Bierman, 1986), especially with regard to the optimal proportion of carbohydrate-containing foods. The nutritional requirements of people with diabetes are essentially
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Page 629 the same as those for the general population. Restriction of total caloric intake to achieve ideal body weight is the primary dietary intervention recommended for NIDDM (NIH, 1986). Restriction of fat intake to £ 30% calories is also advised, and reduced intake of saturated fatty acids and dietary cholesterol (see Chapter 7) is advisable because of the very high rate of mortality from atherosclerotic coronary diseases among those with IDDM and NIDDM (Krowlewski et al., 1987; National Diabetes Data Group, 1985; West 1978). Carbohydrates from vegetables and fruits are usually substituted for fats in the diet of diabetic patients (American Diabetes Association, 1987). There is some recent evidence that simple sugars such as sucrose need not be restricted (Bantle et al., 1983; Chantelau et al., 1985; Jellish et al., 1984; Peterson et al., 1986; Slama et al., 1984). There is no clear consensus, however, on this issue as well as on the proportion of carbohydrate needed in the diet for the management of diabetes mellitus (Garg et al., 1988; Jarrett, 1981; Nuttall, 1983; Reaven, 1980; Wood and Bierman, 1986). Reaven and colleagues caution against using a high-carbohydrate diet for long-term management of NIDDM because it can increase levels of postprandial glucose, insulin, and basal triglycerides (Coulston et al., 1987; Reaven, 1988). Other studies show wide variation in the glucose response to simple sugars and to foods containing complex carbohydrates (Crapo, 1985; Crapo et al., 1981; Jenkins et al., 1981). Soluble dietary fiber, including guar, pectin, and oat bran, lowers plasma glucose levels among people with diabetes (Anderson et al., 1984; see also Chapter 10). However, the use of purified fiber supplements is not recommended for diabetes therapy since evidence of long-term efficacy and safety is lacking (NIH, 1986). People with diabetes mellitus appear to have no special requirements for protein. There is increasing concern, however, that high protein intakes may be associated with increased risk of renal disease (diabetic nephropathy) in IDDM and NIDDM. Ciavarella (1987) reported that a 4- to 5-month dietary protein restriction in the diet of seven IDDM patients with early clinical nephropathy reduced albuminuria. This subject needs further investigation. Hypertension appears to accelerate the progression of nephropathy in diabetics. The role of reduced sodium intake in slowing progression of this disorder remains to be elucidated (see Chapter 20). Animal Studies In normal strains of animals, it has been difficult to prove a specific effect of total caloric intake or the intake of specific nutrients on the emergence of diabetes mellitus (Glinsmann et al., 1986). As discussed in Chapter 6, large increases in total food intake that lead to adiposity in animals also lead to an increased incidence of insulin resistance (see section on total caloric intake and obesity in Chapter 6) (Hallfrisch et al., 1981; Johnson et al., 1975; Romsos and Leveille, 1974; Stem et al., 1975; Susini and Lavau, 1978; Turkenkopf et al., 1982) and some other aspects of NIDDM seen in humans. The metabolic responses to increased total caloric intake usually become apparent only over a relatively long period. Thus, many of the animal studies of putative dietary-induced diabetes are confounded not only by the adiposity resulting from overfeeding, but also by the effects of aging inherent in long-term dietary studies. In most cases, the effects of increased caloric intake on insulin resistance can be reversed by weight reduction and restoration of a more normal body weight. Thus, it is difficult to separate any specific effect of calories on the development of diabetes from their effects on overall adiposity. There are several animal models for studying the genetics of NIDDM and IDDM, particularly among rodents (Salans and Graham, 1982). Although there is some evidence that excessive consumption of certain nutrients may enhance (Cohen, 1978; Leiter et al., 1983) or provoke (Coleman, 1982; Greenwood et al., 1988; Ikeda et al., 1981) the appearance of incipient diabetes and exacerbate some pathological conditions (see Chapter 9), there is little evidence that the diabetic condition depends upon hyperphagia or ingestion of certain nutrients. One exception to this is the sand rat, which normally remains lean and nondiabetic in the wild but when housed under laboratory conditions becomes hyperphagic and often diabetic (Kalderon et al., 1986; Rice and Robertson, 1980). There is some evidence that dietary fiber may modulate the expression of hyperglycemia in chemically induced and spontaneous diabetes in rodents (see Chapter 10). Diabetes mellitus can be induced experimentally in several ways, e.g., by the injection of streptozotocin or alloxan (beta-cell toxins) or by the surgical extirpation of all or part of the pancreas. Hypoinsulinemia follows such treatment and usually precedes any increase in food intake (although polyphagia may occur with polydipsia). Marked
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Page 630 changes in the dietary preferences of diabetic rodents occur later and are not etiologically implicated in the initiation of the diabetes syndrome; they may, in fact, be symptoms of adaptation (Friedman, 1978; Kanarek et al., 1980). Summary Relative body weight seems to be the only factor that has been consistently related to the prevalence of NIDDM, which is associated directly with the mean percentage of calories from fats and inversely with the mean percentage of calories from carbohydrates. This finding is attributed to the greater caloric density of high-fat diets rather than to any specific action of the nutrient itself. Fiber intake does not appear to be associated with the risk of developing NIDDM. Alcohol intake has been correlated with hyperglycemia, and ethanol is believed to impair glucose tolerance. The possible role of chromium deficiency in the etiology of diabetes is unresolved. There is no evidence that dietary composition influences the risk of developing diabetes mellitus. Directions for Research The following areas need further investigation: · Basic mechanisms through which genetic and dietary factors interact in the etiology of diabetes mellitus. · The role of high carbohydrate diets with varying amounts and types of carbohydrates and fats in the long-term management of diabetes mellitus and its complications. · The role of gene-environment interaction in NIDDM. · Methods for reducing obesity and maintaining normal body weight in alleviating diabetes and its complications, and the nutritional, environmental, behavioral, and genetic aspects of obesity in the etiology of NIDDM. · The role of saturated fatty acids and dietary cholesterol in mortality from coronary heart disease in people with diabetes. · The role of protein intake in chronic renal failure in people with diabetes. · The role of dietary fiber in reducing the risk of diabetes. References American Diabetes Association. 1987. Nutritional recommendations and principles for individuals with diabetes mellitus: 1986. Diabetes Care 10:126-132. Anderson, J.W., L. Story, B. Sieling, W.J. Chen, M.S. Petro, and J. Story. 1984. Hypocholesterolemic effects of oat-bran or bean intake for hypercholesterolemic men. Am. J. Clin. Nutr. 40:1146-1155. Anderson, R.A. 1986. Chromium metabolism and its role in disease processes in man. Chem. Physiol. Biochem. 4: 31-41. Bantle J.P., D.C. Laine, J.W. Castle, J.W. Thomas, B.J. Hoogwerf, and F.C. Goetz. 1983. Postprandial glucose and insulin responses to meals containing different carbohydrates in normal and diabetic subjects. N. Engl. J. Med. 309:7-12. Barnett, A.H., C. Eff, R.D.G. Leslie, and D.A. Pyke. 1981. Diabetes in identical twins. Diabetologia 70:87-93. Bierman, E.L. 1979. Nutritional management of adult and juvenile diabetics. Pp. 107-117 in M. Winick, ed. Nutritional Management of Genetic Disorders. Wiley, New York. Callaway, C.W., and A.A. Rossini. 1987. Diabetes mellitus. Pp. 764-793 in W.T. Branch, Jr., ed. Office Practice of Medicine, 2nd ed. W.B. Saunders, Philadelphia. Chantelau, E.A., G. Gösseringer, G.E. Sonnenberg, and M. Berger. 1985. Moderate intake of sucrose does not impair metabolic control in pump-treated diabetic out-patients. Diabetologia 28:204-207. Ciavarella, A., G. DiMizio, S. Stefoni, L.C. Borgnino, and P. Vannini. 1987. Reduced albuminuria after dietary protein restriction in insulin-dependent diabetic patients with clinical nephropathy. Diabetes Care 10:407-413. Cohen, A.M. 1978. Genetically determined response to different ingested carbohydrates in the production of diabetes. Horm. Metab. Res. 10:86-92. Coleman, D.L. 1982. Diabetes-obesity syndromes in mice: proceedings of a task force on animals appropriate for studying diabetes mellitus and its complications. Diabetes 31 suppl. 1:1-6. Coulston, A.M., C.B. Hollenbeck, A.L.M. Swislock, Y.D.I. Chen, and G.M. Reaven. 1987. Deleterious metabolic effect of high carbohydrate, sucrose-containing diets in patients with non-insulin-dependent diabetes mellitus. Am. J. Med. 82:213-220. Crapo, P.A. 1985. Simple vs. complex carbohydrate in the diabetic diet. Annu. Rev. Nutr. 5:95-114. Crapo, P.A., J. Insel, M. Sperling, and O.G. Kolterman. 1981. Comparison of serum glucose, insulin, and glucagon responses to different types of complex carbohydrate in noninsulin-dependent diabetic patients. Am. J. Clin. Nutr. 34:184-190. Friedman, M.I. 1978. Hyperphagia in rats with experimental diabetes mellitus: a response to decreased supply of utilizable fuels. J. Comp. Physiol. Psychol. 92:109-117. Garg, A., A. Bonanome, S.M. Grundy, Z.J. Zhang, and R.H. Unger. 1988. Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus. N. Engl. J. Med. 310:829-839. Gerard, M.J., A.L Klatsky, A.B. Siegelaub, G.B. Friedman, and R. Feldman. 1977. Serum glucose levels and alcohol-consumption habits in a large population. Diabetes 26:780-785. Glinsmann, W.H., H. Irausquin, and Y.K. Park. 1986. Evaluation of health aspects of sugars contained in carbohydrate sweeteners: report of Sugars Task Force, 1986. J. Nutr. 116:S1-S216. Greenwood, M.R.C., R. Kava, D.B. West, and V.A. Lukasik. 1988. Wistar fatty rat: a sexually dimorphic model of human noninsulin-dependent diabetes. Pp. 316-318 in E. Shafrir and A.E. Renold, eds. Frontiers in Diabetes Research: Lessons from Animal Diabetes II. John Libbey, London.
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Page 631 Hallfrisch, J., L. Cohen, and S. Reiser. 1981. Effects of feeding rats sucrose in a high fat diet. J. Nutr. 111:531-536. Ikeda, H., A. Shino, T. Matsuo, H. Iwatsuka, and Z. Suzuoki. 1981. A new genetically obese-hyperglycemic rat (Wistar fatty). Diabetes 30:1045-1050. Jarrett, R.J. 1981. More about carbohydrate. Diabetologia 21: 427-429. Jellish, W.S., M.A. Emanuele, and C. Abraira. 1984. Graded sucrose/carbohydrate diets in overtly hypertriglyceridaemic diabetic patients. Am. J. Med. 77:1015-1022. Jenkins, D.J.A., D.V. Goff, A.R. Leeds, K.G.M.M. Alberti, T.M.S. Wolever, M.A. Gassull, and T.D.R. Hockaday. 1976. Unabsorbable carbohydrates and diabetes: decreased post-prandial hyperglycemia. Lancet 2:172-174. Jenkins, D.J.A., T.M.S. Wolever, R. Nineham, R. Taylor, G.L. Metz, S. Bacon, and T.D.R. Hockaday. 1978. Guar crisp bread in the diabetic diet. Br. Med. J. 2:1744-1746. Jenkins, D.J.A., R.H. Taylor, R. Nineham, D.V. Goff, S.R. Bloom, D. Sarson, and K.G.M.M. Alberti. 1979. 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Ethnic differences in susceptibility to non-insulin-dependent diabetes. A comparative study of two urbanized Micronesian populations. Diabetes 33:1002-1007. Krowlewski, A.S., E.J. Kosinski, J.H. Warran, O.S. Leland, E.J. Busick, A.C. Asmal, L.F. Rand, A.R. Christlieb, R.F. Bradley, and C.R. Kahn. 1987. Magnitude and determinants of coronary artery disease in juvenile-onset, insulin-dependent diabetes mellitus. Am. J. Cardiol. 59:750-755. Leiter, E.H., D.L. Coleman, D.K. Ingram, and M.A. Reynolds. 1983. Influence of dietary carbohydrate on the induction of diabetes in C57BI/KsJ-db/db diabetic mice. J. Nutr. 113:184-195. LSRO (Life Sciences Research Office). 1987. Physiological Effects and Health Consequences of Dietary Fiber. Federation of American Societies for Experimental Biology, Bethesda, Md. 236 pp. Monnier, L., T.C. Pham, L. Aguirre, A. Orseffi, and J. Mirouze. 1978. Influence of indigestible fibers on glucose tolerance. Diabetes Care 1:83-88. Morgan, L.M., T.J. Goulder, D. Tsiolakis, V. Marks, and K.G.M.M. Alberti. 1979. The effect of unabsorbable carbohydrate on gut hormones: modification of post-prandial GIP secretion by guar. Diabetologia 17:85-89. National Diabetes Data Group. 1985. Diabetes in America: Diabetes Data Compiled 1984. NIH Publ. No. 85-1468. National Institute of Arthritis, Diabetes and Digestive and Kidney Diseases, National Institutes of Health. Public Health Service, U.S. Department of Health and Human Services, Bethesda, Md. (various pagings). NIH (National Institutes of Health). 1986. Diet and exercise in noninsulin-dependent diabetes mellitus. National Institutes of Health Consensus Development Conference Statement, Vol. 6. National Institute of Arthritis, Diabetes and Digestive and Kidney Diseases and the Office of Medical Applications of Research. U.S. Department of Health and Human Services, Bethesda, Md. 21 pp. Nuttall, F.Q. 1983. Diet and the diabetic patient. Diabetes Care 6:197-207. Peterson, D.B., J. Lambert, S. Gerring, D.P. Darling, R.D. Carter, R. Jelfs, and J.I. Mann. 1986. Sucrose in the diet of diabetic patientsjust another carbohydrate? Diabetologia 29:216-220. Poynard, T., G. Slama, A. Delage, and G. Tchobroutsky. 1980. Pectin efficacy in insulin-treated diabetics assessed by the artificial pancreas. Lancet 1:158. Rabinowitz, M.B., H.C. Gonick, S.R. Levin, and M.B. Davidson. 1983. Effects on chromium and yeast supplements on carbohydrates and lipid metabolism in diabetic men. Diabetes Care 6:319-327. Reaven, G.M. 1980. How high the carbohydrate? Diabetologia 19:409-413. Reaven, G.R. 1988. Dietary therapy for non-insulin dependent diabetes mellitus. N. Engl. J. Med. 319:862-864. Riales, R.M., and J. Albrink. 1981. Effect of chromium chloride supplementation on glucose tolerance and serum lipids including high-density lipoprotein of adult men. Am. J. Clin. Nutr. 34:2670-2678. Rice, M.C., and R.P. Robertson. 1980. Re-evaluation of the sand rat as a model of diabetes mellitus. Am. J. Physiol. 239:E340-E345. Romsos, D.R., and G.A. Leveille. 1974. Effect of meal frequency and diet composition on glucose tolerance in the rat. J. Nutr. 104:1503-1512. Salans, L., and B. Graham, eds. 1982. Proceedings of a task force on animals appropriate for studying diabetes mellitus and its complications. Diabetes 31 suppl. 1:1-102. Simonoff, M. 1984. Chromium deficiency and cardiovascular risk. Cardiovasc. Res. 18:591-596. Slama, G., M.J. Haarat, P. Jean-Joseph, D. Costagliola, I. Goicolea, F. Bornet, F. Elgrably, and G. Tchobroutsky. 1984. Sucrose taken during a mixed meal has no additional hyperglycaemic action over isocaloric amounts of starch in well-controlled diabetics. Lancet 2:122-125. Stern, J.S., P.R. Johnson, B.R. Batchelor, L.M. Zucker, and J. Hirsch. 1975. Pancreatic insulin release and peripheral tissue resistance in Zucker obese rats fed high- and low-carbohydrate diets. Am. J. Physiol. 228:543-548. Susini, C., and M. Lavau. 1978. In vitro and in vivo responsiveness of muscle and adipose tissue to insulin in rats rendered obese by a high-fat diet. Diabetes 27:114-120. Turkenkopf, I., P.R. Johnson, and M.R.C. Greenwood. 1982. Development of pancreatic and plasma insulin in prenatal and suckling Zucker rats. Am. J. Physiol. 242:E220-E229. West, K.N. 1978. Epidemiology of Diabetes and Its Vascular Lesions. Elsevier/North-Holland, New York. 579 pp. Wood, F.C., Jr., and E.L. Bierman. 1986. Is diet the cornerstone of management of diabetes? N. Engl. J. Med. 315:1224-1227. Yki-Järvinen, H., and E.A. Nikkilä. 1985. Ethanol decreases glucose utilization in healthy man. J. Clin. Endocrinol. Metab. 61:941-945.
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