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The author discusses the very low calorie diet and its physiopathological effects, in the treatment of NIDDM with obesity. In the latter condition the very low calorie diet can be utilized in order to obtain the desired body weight decrease, and consequently to improve glucose tolerance; however, this goal can only be reached by including in the diet sufficient amounts of carbohydrates, and by following some identified parameters of the treated patient.
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PMID:[Semifasting and type II diabetes mellitus]. 219 12

This report presents an overview of the prevalence, characteristics, morbidity, mortality, and risk factors for noninsulin-dependent diabetes (NIDDM) in Blacks and Whites in the United States. Data are drawn primarily from national surveys, but the report also includes the few clinical studies that have differentiated the two races. NIDDM constitutes 90-95% of all diabetes in the United States and is more prevalent in Black Americans than in Whites. Diabetes prevalence increases with age for both races and reaches 26% among Blacks aged 65-74 years compared with 18% among Whites. Rates of diabetes among persons aged 20-74 years are 30% higher in White women, 70% higher in Black men, and 100% higher in Black women, compared with White men. Approximately half of diabetes is undiagnosed in both races. White and Black diabetics are similar with regard to age, duration of diabetes, and diabetes therapies, although Blacks of both sexes are more obese than their White counterparts. Rates of vision loss, amputations, and renal disease are 1.5-4 times higher in Blacks than in Whites, although prevalence of hypertension is about equal in the two races. Blacks and Whites see the same physician specialists for their diabetes, but Whites have approximately 40% more visits to office-based physicians each year. Diabetes-specific mortality has declined significantly in the past decade and may now be lower in Black than in White diabetics. Risk factors for diabetes, including age, sex, obesity, and family history of diabetes, all operate within both race groups and probably interact with each other. The effect of gender and family history on rates of diabetes is similar in Blacks and Whites. Blacks have higher rates of diabetes at each obesity level, indicating that obesity alone cannot explain the differential in prevalence between the races. Impaired glucose tolerance (IGT), a strong risk factor for development of diabetes, increases with age in all race/sex groups except for Black women older than 54 years in whom rates of IGT, decline, possibly because of conversion of IGT to diabetes.
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PMID:Noninsulin-dependent diabetes mellitus in black and white Americans. 219 51

There are three major obstacles to a recommendation for screening the elderly for NIDDM. The first is the conflicting evidence as to whether early detection and treatment reduce complications. The second is that treatment of hyperglycemia with attainment of euglycemia is difficult to achieve in the elderly. Nondrug therapy often fails because of lifelong eating habits, denture problems, fixed income, and physical handicaps. Drug therapy is fraught with the dangers of hypoglycemia and drug interactions. Compliance with therapy often is poor and leads to conflicts between physician and patient that may be detrimental in the treatment of other diseases in which intervention has proven worthwhile. The third obstacle is the lack of data regarding the adverse effects of labeling and noncompliance issues in the face of a positive screening test. Because obesity is a risk factor for NIDDM and hypertension in conjunction with NIDDM leads to atherosclerosis, screening and treatment for these two conditions are warranted whether or not NIDDM is present concurrently. Medicine is in a dynamic state of flux and, undoubtedly, conflicts over the benefits of early treatment and patient compliance will be resolved. Until then, there is no justification for screening for NIDDM in the elderly.
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PMID:Screening for non-insulin-dependent diabetes mellitus in the elderly. 222 50

The mean additional energy requirement for pregnancy has been calculated at 285 kcal daily and it reflects the energy needs for production of the fetoplacental unit and for the maternal physiological adaptations to pregnancy. In practice there is considerable variation in energy requirement due to alterations in maternal energy expenditure. Optimal energy intakes are dictated also by the pre-pregnancy maternal weight. The outcome of pregnancy is improved in the underweight mother by an intake which produces a weight gain in pregnancy of approximately 14 kg, whereas a rise of only 7 kg may be optimal for the obese mother. Obesity with or without diabetes is associated with macrosomia and other problems and it is sensible to attempt to limit weight gain in pregnancy at a time when maternal motivation is high. Diabetes in pregnancy may arise in patients with pre-existing NIDDM or IDDM, but more commonly it is diagnosed for the first time during pregnancy and it usually disappears after delivery (gestational diabetes). Recent evidence suggests that gestational diabetes has a strong genetic component and is usually NIDDM precipitated early in life by the pregnancy. Both gestational diabetes and NIDDM are characterized by insulin deficiency and by insulin resistance. Long-term follow-up studies have demonstrated that NIDDM or impaired glucose tolerance develop in later life in 50-70% of women with previous gestational diabetes. The adverse effects of pregnancy on the mother with pre-existing diabetes may be minimized by good diabetic control as may be adverse effects on the fetus and neonate of diabetes in the mother. An increased incidence of fetal malformations persists in pregnancies with pre-existing maternal diabetes. Diabetes of any form may be associated with neonatal hypoglycaemia. The aim of therapy is to produce maternal normoglycaemia throughout pregnancy by dietary measures and insulin treatment if required. Women with pre-existing diabetes should tighten their blood glucose control from before conception. Optimization of insulin therapy and diet are required for IDDM and most NIDDM women will require insulin treatment in pregnancy. Gestational diabetics require diet and possibly insulin. Most pregnancies now proceed to term.
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PMID:Diabetes and diet in pregnancy. 224 97

We studied the association of obesity with serum lipid and lipoprotein concentrations in 117 patients (62 males and 55 females) with NIDDY and in 40 nondiabetic control subjects (21 males and 19 females). Obesity at a young age was related to increased lipid and lipoprotein levels both in the patients with NIDDM and the control group. Moreover, low HDL-c levels were aggravated by diabetic status only in males. The BMI and fasting insulin level had a statistically significant correlation with the TG and HDL-c level and various atherogenic factors. Therefore, it is suggested that the lipid abnormalities seen in obesity may be associated with hyperinsulinemia. We conclude that obesity in adolescence leads to aberrations of the serum lipid and lipoprotein levels, particularly in obese males with NIDDY.
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PMID:Adverse effects of obesity on lipid and lipoprotein levels in the patients with non-insulin dependent diabetes in the young. 228 36

We studied the association of obesity with lipid and lipoprotein concentrations in 92 patients (49 men, 43 women) with insulin-dependent diabetes (IDDM), in 305 patients (152 men, 153 women) with non-insulin-dependent diabetes (NIDDM), and in 122 nondiabetic control subjects (65 men, 57 women). Obesity (body mass index, BMI) was associated with abnormal lipid and lipoprotein levels only in the presence of diabetes, and lipid and lipoprotein changes were substantially more abnormal in patients with NIDDM than in patients with IDDM. In men and women with NIDDM, obesity was associated with low high-density lipoprotein (HDL) and HDL2 cholesterol and high total, low-density lipoprotein (LDL), and very low-density lipoprotein (VLDL) triglyceride concentrations. In men with IDDM, obesity was related only to low HDL and HDL2 cholesterol and in women with IDDM to low HDL3 cholesterol. BMI and diabetes status had a statistically significant interaction (analysis of variance) with respect to HDL and HDL2 cholesterol and total and VLDL triglycerides, indicating that the effects of obesity on lipids and lipoproteins were more severe in patients with diabetes than in nondiabetic subjects. In conclusion, obesity and diabetes status have an unfavorable interaction that results in multiple pathologic lipid and lipoprotein changes, particularly in NIDDM.
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PMID:Adverse effects of obesity on lipid and lipoprotein levels in insulin-dependent and non-insulin-dependent diabetes. 229 84

In order to assess to what extent familial factors play a role in thermogenesis of obese individuals, the 3 h response to a 100 g glucose oral load was measured in 11 obese subjects (6 m, 5 f) with a familial history of obesity and/or obesity-non-insulin dependent diabetes mellitus (NIDDM, group A); these were compared to 9 obese subjects (5 m, 4 f) without familial history of these disorders (group B). All subjects had normal glucose tolerance and the two groups were comparable with respect to anthropometric features. The glucose-induced thermogenesis of group A (7.9 +/- 1.2 per cent) above preload energy expenditure was significantly lower (P less than 0.01) than that observed in group B (13.5 +/- 0.5 per cent). The same conclusions were obtained when the results were expressed as a percentage of the glucose load ingested (4.4 +/- 0.67 and 7.8 +/- 0.80 in group A and group B respectively, P less than 0.01). Despite these differences the pattern of change in glycaemia, insulinaemia, C-peptidaemia and glucagonaemia in response to the glucose load was the same between the two groups. Total glucose oxidation as well as non-oxidative glucose disposal did not differ between the two groups. These results seem to support the hypothesis that genetic factors may contribute to the low thermogenic response observed in some individuals with a familial history of obesity and/or obesity-NIDDM.
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PMID:Glucose-induced thermogenesis in obese subjects with or without familial history of obesity. 238 74

Parameters of fibrinolysis, including euglobulin fibrinolytic activity, tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PA-inhibitor) activity, and plasmin-alpha 2-antiplasmin complex (PAP) were studied in 62 patients (35 women and 27 men; ages 53 +/- 16 years) with either insulin-dependent (IDDM) or noninsulin-dependent (NIDDM) diabetes mellitus. Compared to a control group of similar age (n = 57), the diabetic patients had a significantly lower mean euglobulin fibrinolytic activity (1.2 +/- 0.7 vs. 1.7 +/- 1.1 ng/ml, p less than 0.01) but significantly higher mean t-PA antigen (15.7 +/- 8.4 vs. 6.6 +/- 2.9 ng/ml, p less than 0.001) and PA-inhibitor activity (2.6 +/- 1.3 vs. 1.5 +/- 0.7 IU/ml, p less than 0.001) levels. Significant univariate correlations were observed between PA-inhibitor activity and age (r = 0.32, p less than 0.05), diastolic blood pressure (r = 0.42, p less than 0.01) and euglobulin fibrinolytic activity (r = -0.40, p less than 0.01). In multivariate analysis, only body mass index (positively) and euglobulin fibrinolytic activity (negatively) remained significantly related to PA-inhibitor activity in the total diabetic population as well as in the NIDDM group. The only parameter in the IDDM group significantly related to PA-inhibitor activity was diastolic blood pressure. These results suggest that PA-inhibitor plays a role in the regulation of fibrinolysis in diabetes patients and that factors like obesity and hypertension may be related to reduced fibrinolysis via PA-inhibitor levels.
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PMID:Tissue-type plasminogen activator antigen and plasminogen activator inhibitor in diabetes mellitus. 244 56

Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. We have examined restriction fragment length polymorphisms (RFLPs) near "candidate diabetogenic genes" as one approach to identify molecular markers for GDM genes. Genotypes for insulin hypervariable region (HVR), insulin-like growth factor II (IGF2), insulin receptor (INSR), and glucose transporter (GLUT1) RFLPs were studied in 96 GDM and 164 control subjects, matched to GDM for race, age, and gravidity. Logistic regression analysis was used to explore the relationship between genotypes at these candidate gene loci and GDM, while adjusting for the effects of potential confounding variables. Among black subjects, the INSR allele 1 (P = 0.001) and interactions between INSR allele 1 with body mass index (BMI) (P = 0.002) and history of DM in subject's mother (P = 0.004) contributed significantly to GDM risk. Among Caucasian subjects, a similar relationship between the INSR allele 1 (P = 0.007) and INSR allele 1-BMI interactions (P = 0.011) on GDM risk were observed. In Caucasians, an additional significant risk factor was determined by an INSR allele 1-IGF2 allele 2 interaction (P = 0.018). No risk factors were identified in Hispanic subjects. These data continue to support the hypothesis that GDM is a heterogeneous disorder with respect to phenotypic and genotypic features. Furthermore, our data suggest that risk for GDM in black and Caucasian subjects is not due to obesity perse but to interactions between obesity and INSR alleles. In Caucasian women, INSR and IGF2 alleles interact to confer additional risk for GDM. Thus genes underlying susceptibility to GDM in some women may be similar to genes conferring risk to NIDDM, while in others novel genes may contribute to GDM risk.
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PMID:Increased risk for gestational diabetes mellitus associated with insulin receptor and insulin-like growth factor II restriction fragment length polymorphisms. 257 27

The Garg study diet supplied 50% of the calories from fat (33% from monounsaturated fat), which eliminates much of the bulk from the diet. Substituting monounsaturates for carbohydrates in the diet translates into giving up 120 calories from a carbohydrate source (very large potato, 1 1/2 slices of bread, 1 cup of cereal, etc) for a tablespoon of olive oil. Somehow that doesn't seem like a good exchange. Abbott et al substituted complex carbohydrates for saturated fat in the diet and accomplished the same result as Coulston et al with a low-carbohydrate (40%), moderate-fat (40%) diet. The American Diabetes Association suggested that if diabetes was poorly controlled and hypertriglyceridemia a problem, monounsaturates might be useful to maintain caloric balance. However, in light of the high incidence of obesity in persons with NIDDM and recent studies on the ease of dietary fat storage in adipose tissue, should fat of any kind, including monounsaturated fats, be substituted for carbohydrates in the diet of persons with diabetes?
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PMID:How enthusiastically should the use of monounsaturated fats be encouraged? 262 65


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