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Carbohydrate counting is a meal planning approach used with clients who have diabetes that focuses on carbohydrate as the primary nutrient affecting postprandial glycemic response. The concept of carbohydrate counting has been around since the 1920s, but it received renewed interest after being used as 1 of 4 meal planning approaches in the Diabetes Control and Complications Trial. In the trial, carbohydrate counting was found to be effective in meeting outcome goals and allowed flexibility in food choices. Recent practice pattern surveys have shown an increasing interest in and use of carbohydrate counting for medical nutrition therapy for persons with diabetes. Carbohydrate counting can be used by clients with type 1, type 2, and gestational diabetes. Three levels of carbohydrate counting have been identified based on increasing levels of complexity. Level 1, or basic, introduces clients to the concept of carbohydrate counting and focuses on carbohydrate consistency. Level 2, or intermediate, focuses on the relationships among food, diabetes medications, physical activity, and blood glucose level and introduces the steps needed to manage these variables based on patterns of blood glucose levels. Level 3, or advanced, is designed to teach clients with type 1 diabetes who are using multiple daily injections or insulin infusion pumps how to match short-acting insulin to carbohydrate using carbohydrate-to-insulin ratios. All 3 levels emphasize portion control and offer opportunities for using creative teaching methods, such as "food labs," and use of a variety of carbohydrate resource tools and publications. In this article, glycemic effects of protein, fat, and fiber intake are discussed for persons with type 1 and type 2 diabetes. Decision trees are introduced for each level of carbohydrate counting and show the usual progression through each level. Carbohydrate counting as a meal planning approach offers variability of food choices with the potential for improving glycemic control. Research opportunities are available for those interested in comparing carbohydrate counting with other meal planning approaches for clients with diabetes and the effects on clinical outcomes.
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PMID:Using carbohydrate counting in diabetes clinical practice. 971 Jun 60

Despite the fact that it is the prevalent view that insulin resistance is the main genetic factor predisposing to development of type 2 diabetes, review of several lines of evidence in the literature indicates a lack of overwhelming support for this concept. In fact, the literature better supports the case of impaired insulin secretion being the initial and main genetic factor predisposing to type 2 diabetes, especially 1) the studies in people at high risk to subsequently develop type 2 diabetes (discordant monozygotic twins and women with previous gestational diabetes), 2) the studies demonstrating compete alleviation of insulin resistance with weight loss, and 3) the studies finding that people with type 2 diabetes or IGT can have impaired insulin secretion and no insulin resistance compared with well matched NGT subjects. The fact that insulin resistance may be largely an acquired problem in no way lessens its importance in the pathogenesis of type 2 diabetes. Life style changes (exercise, weight reduction) and pharmacological agents (e.g., biguanides and thiazolidendiones) that reduce insulin resistance or increase insulin sensitivity clearly have major beneficial effects (122, 144-146, 153-155).
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PMID:The genetic basis of type 2 diabetes mellitus: impaired insulin secretion versus impaired insulin sensitivity. 971 77

The most common types of diabetes observed in a primary care practice are type 1, type 2, and gestational diabetes. Type 1 diabetes is an autoimmune disease characterized by total destruction of the pancreatic beta cells, whereas insulin resistance, impaired insulin secretion, and inappropriate hepatic glucose secretion characterize type 2 diabetes. Gestational diabetes is similar to type 2 diabetes, but is first diagnosed during pregnancy.
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PMID:Pathophysiology of diabetes mellitus. 975 16

Type 2 diabetes is a major public health concern for people of color throughout the United States. The prevalence of type 2 diabetes among African-Americans, Hispanics and American Indian/Alaskan Natives is from two to six times greater than that of the US non-Hispanic white population. Rates of end-stage renal disease, amputations, and diabetic retinopathy are also significantly higher. The medical risk factors of familial history, insulin resistance, obesity, history of gestational diabetes, impaired glucose tolerance, and physical inactivity are the same for all populations. The disproportionate impact of diabetes in people of color may be because of an interaction of genetic risk factors and environmental factors. Recognizing the impact of culture in disease management and self-care practices can improve diabetes care.
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PMID:Type 2 diabetes in people of color. 975 26

In July 1997, the American Diabetes Association (ADA) has published new recommendations for the diagnosis and classification of diabetes mellitus. Except for gestational diabetes they should be identical to the new WHO recommendations (not yet published). From now on, only the fasting glucose should be used for clinical routine. The oral glucose tolerance test is no longer recommended for this purpose. The diagnostic cut-off level for fasting glucose was decreased from 140 mg/100 ml (venous plasma) to 126 mg/dl, and the range between 110 and 125 mg/100 ml was defined as impaired fasting glucose (IFG), a new diagnostic category introduced in analogy to impaired glucose tolerance (IGT). The lower diagnostic cut-off level for fasting glucose has been proposed because the risk of developing diabetic late complications (predominantly at the vascular system) is already increased in blood glucose ranges thought to be normal. The diagnostic criteria for gestational diabetes are unchanged and still discrepant between ADA and WHO. The two major forms of diabetes should be designated only as type 1- and type 2-diabetes with respect to etiology and pathogenesis. Type 1-diabetes was subdivided into an immune-mediated and into an idiopathic form. MODY (maturity-onset type diabetes in young people) was listed separately from type 2-diabetes under the category of genetic defects of beta-cell function, also mitochondrial diabetes (maternally inherited diabetes and deafness). Malnutrition-related diabetes has been omitted as a major form of diabetes.
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PMID:[Modern diagnosis and classification of diabetes mellitus]. 984 90

Zeeburg', a multiethnic town borough in the Amsterdam-East region, has one of the city's highest rates of immigrants. In the total population of 19,825 Surinam (mainly Creole), Turkish, Moroccan, and Dutch adults the prevalence of known type 2 diabetes in 1994 and of gestational diabetes mellitus (GDM) between January 1992 and January 1997 was investigated. Based on World Health Organization (WHO) criteria of 1985, the age-standardized prevalence of type 2 diabetes was similar in men (6.4%; 95% confidence interval [CI]: 5.6-7.2) and women (6.4%: 95% CI: 5.8-7.0) for all ethnic groups combined. However, the age- and sex-standardized prevalence of type 2 diabetes was significantly greater in the non-Dutch inhabitants than in the Dutch inhabitants (17.3% [95% CI: 12.9-21.6] in Surinam inhabitants, 10.9% [95% CI: 9.7-12.2] in Turkish inhabitants, 12.4% [95% CI: 9.7-15.0] in Moroccan inhabitants, and 3.6% [95% CI: 3.2-3.9] in Dutch inhabitants). The odds ratios for type 2 diabetes for the separate immigrant groups relative to the Dutch group were 5.88 (95% CI: 4.54-7.69) for Surinam inhabitants, 4.00 (95% CI: 2.86-5.55) for Turkish inhabitants, and 4.17 (95% CI: 3.03-5.55) for Moroccan inhabitants. GDM was present in 2.59% of women of non-Dutch origin compared with 0.62% of women of Dutch origin. A significant positive association was found between the non-Dutch origin and the occurrence of GDM (chi2 = 6.7; p < 0.01). The study highlights a high prevalence of known type 2 diabetes and GDM in the immigrant inhabitants and emphasizes that appropriate interventions are necessarily with implications for health targets and capitation based budgets.
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PMID:The prevalence of type 2 diabetes and gestational diabetes mellitus in an inner city multi-ethnic population. 984 31

GDM develops in 1-3% of all pregnancies. Women with GDM are characterized by a relatively diminished insulin secretion coupled with a pregnancy-induced insulin resistance primary located in skeletal muscle tissue. The cellular background for this insulin resistance is not known. The binding of insulin to its receptor and the subsequent activation of the insulin receptor tyrosine kinase have significant importance for the cellular effect of insulin. Thus, the pathogenesis to the insulin resistance was studied by investigating insulin receptor binding and tyrosine kinase activity in skeletal muscle biopsies from women with GDM and pregnant controls. No major abnormalities were found in GDM wherefore it is likely that the insulin resistance is caused by intracellular defects distal to the activation of the tyrosine kinase. Glucose tolerance returns to normal postpartum in the majority of women with GDM. However, previous studies, in populations quite different from a Danish population, have shown that women with previous GDM have a high risk of developing overt diabetes mellitus later in life. Hence, we aimed to investigate the prognosis of women with previous GDM with respect to subsequent development of diabetes and also to identify predictive factors for the development of overt diabets in these women. A follow-up study of diet treated GDM women diagnosed during 1978 to 1985 at the Rigshospital, Copenhagen was performed. Glucose tolerance was evaluated in 241 women (81% of the GDM population) 2-11 years after pregnancy. Abnormal glucose tolerance was found in 34.4% of the women (3.7% IDDM, 13.7% NIDDM, 17% IGT) in contrast to a control group where none had diabetes and 5.3% had IGT. Logistic regression analysis identified the following independent risk factors for later development of diabetes: a high fasting glucose level at diagnosis of GDM, a delivery more than 3 weeks before term, and an abnormal OGTT 2 months postpartum. Low insulin secretion at diagnosis of GDM was also an independent risk factor. The presence of ICA and GAD-autoantibodies in pregnancy was associated with later development of IDDM. In another study the following techniques: hyperinsulinaemic euglycaemic clamp, indirect calorimetry and tritiated glucose infusion were used to evaluate insulin sensitivity in glucose tolerant nonobese women with previous GDM and controls. A decreased insulin sensitivity due to a decreased non-oxidative glucose metabolism in skeletal muscle was found in women with previous GDM. Hence, the activity of three key enzymes in intracellular glucose metabolism (GS, HK and PFK) was studied in skeletal muscle biopsies obtained in the basal state and after 3 h hyperinsulinaemia, with the aim to identify the cellular defects causing the decreased insulin sensitivity. However, no abnormalities in enzyme activity was found. The same group of previous GDM women had a relatively reduced insulin secretion evaluated by the IVGTT. A longitudinal study of 91 GDM women showed a relatively reduced insulin secretion to oral glucose in pregnancy, postpartum as well as 5-11 years later. Thus the present review has shown that even nonobese glucose tolerant women with previous GDM are characterized by the metabolic profile of NIDDM i.e. insulin resistance and impaired insulin secretion. Hence, the combination of this finding together with the significantly increased risk for development of diabetes indicates that all women with previous GDM should have a regular assessment of their glucose tolerance in the years after pregnancy. The first OGTT should be performed around 2 months postpartum in order to diagnose women already diabetic and to identify women with the highest risk for later development of overt diabetes. Women with previous GDM comprise a target group for future intervention trials with the aim to prevent or delay development of NIDDM and IDDM.
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PMID:Gestational diabetes mellitus and subsequent development of overt diabetes mellitus. 985 Aug 11

Within the last 5 years chromium (Cr) has been shown to play a role in glucose intolerance, Type 2 diabetes mellitus (Type 2 DM), and gestational diabetes. In addition, diabetes and the neuropathy of a patient on home parenteral nutrition were alleviated when supplemental Cr was added to total parenteral nutrition (TPN) solutions. In a study conducted in China that has been supported by studies in the United States, supplemental Cr as Cr picolinate improved the blood glucose, insulin, cholesterol, and hemoglobin A1C in people with Type 2 DM in a dose dependent manner. Follow-up studies of > 1 year have confirmed these studies. The requirement for Cr is related to the degree of glucose intolerance: 200 microg/day of supplemental Cr is adequate to improve glucose variables of those who are mildly glucose intolerant. However, people with more overt impairments in glucose tolerance and diabetes usually require more than 200 microg/day. Daily intake of 8 microg of Cr per kg body weight was also more effective than 4 microg/kg in women with gestational diabetes. The mechanism of action of Cr involves increased insulin binding, increased insulin receptor number, and increased insulin receptor phosphorylation. In summary, supplemental Cr has been shown to have beneficial effects without any documented side effects on people with varying degrees of glucose intolerance ranging from mild glucose intolerance to overt Type 2 DM.
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PMID:Chromium, glucose intolerance and diabetes. 985 33

To identify the primary pathogenic factors involved in the development of Type 2 diabetes mellitus (DM), we studied Japanese women with former gestational diabetes mellitus (GDM) who are at risk for the later development of Type 2 DM. We used the minimal model analysis derived from frequently sampled intravenous glucose tolerance test (FSIGT). The subjects consisted of eight non-obese women with a history of GDM and eight non-obese normal women as control subjects. The 75 g oral glucose tolerance test (75 g OGTT) performed within 6 months of delivery confirmed that all the subjects with former GDM had a normal glucose tolerance. Insulin sensitivity (SI) derived from the minimal model analysis was not different between the two groups. Glucose effectiveness at zero insulin (GEZI), reflecting tissue glucose sensitivity, was significantly lower in former GDM patients than in control subjects (1.18+/-0.34 vs 2.26+/-0.29 x 10(-2) min(-1), p < 0.05). The early phase insulin secretion found in FSIGT was markedly reduced to 56% of that observed in control subjects (1250+/-87.4 vs 2223+/-304.3 pmol l(-1) min, p < 0.01). Our results indicate that in former GDM patients, who are japanese and non-obese, impairment of the acute insulin response to glucose and a decrease in tissue glucose sensitivity rather than insulin sensitivity are the primary pathogenic factors involved.
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PMID:No deterioration in insulin sensitivity, but impairment of both pancreatic beta-cell function and glucose sensitivity, in Japanese women with former gestational diabetes mellitus. 986 79

The various types of diabetes mellitus are now more precisely classified according to their etiopathogenies. Therefore, type 1 (autoimmune or not), type 2, gestational diabetes, as well as MODY (Maturity Onset-Diabetes of the Young) and secondary diabetes are considered as separate entities. Any type of diabetes brings its set of complications. Biological chemistry is directed to define the etiopathogenic characteristics of the various types of diabetes and to assess the severity of metabolic and functional disturbances. Diagnostic criteria in term of glycemia have also been reviewed to asses diabetes and glucose intolerance.
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PMID:[Sugar diabetes. Update elements]. 992 23

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