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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied lipid and lipoprotein concentrations and their relationships to insulin level in 994 men and 1246 women ages 50 to 91 years in the upper middle-class community of Rancho Bernardo in southern California. Altogether, 593 men and 741 women had normal glucose tolerance, 240 men and 348 women, impaired glucose tolerance (IGT), 104 men and 117 women, newly diagnosed noninsulin-dependent diabetes (NIDDM), and 57 men and 40 women, previously diagnosed NIDDM. In women but not men, total cholesterol and low density lipoprotein were significantly higher in those with newly diagnosed NIDDM, compared to subjects with normal glucose tolerance. In both men and women, high density lipoprotein (HDL) cholesterol was significantly lower, and total triglyceride significantly higher, in subjects with IGT and NIDDM compared to those with normal glucose tolerance; these differences persisted after adjusting for age, body mass index, smoking, alcohol intake, and exercise level. Multiple linear-regression analyses showed that fasting insulin (but not 2-hour insulin) was significantly associated with low HDL cholesterol and high total triglycerides independently from other variables (age, body mass index, waist/hip ratio, alcohol intake, smoking, exercise, and 2-hour glucose). Overall, these results show that asymptomatic hyperglycemia (IGT, newly diagnosed NIDDM) is associated with lipid and lipoprotein changes favoring atherosclerosis and that fasting hyperinsulinemia (insulin resistance) is the most important factor associated with these lipid and lipoprotein abnormalities
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PMID:Asymptomatic hyperglycemia is associated with lipid and lipoprotein changes favoring atherosclerosis. 267 10

NIDDM is the predominant form of diabetes mellitus in all populations, almost exclusively so in some. Its prevalence varies enormously, with particularly high rates in populations whose lifestyle has drastically changed since World War II. Epidemiologic data from the developed countries of Europe and North America are not adequate to determine whether their incidence rates have also increased. Genetic factors are clearly implicated in the etiology of NIDDM, but their location and mode of expression remain to be determined. The two variables most strongly related to the incidence of NIDDM are age and degree of obesity, although there is emerging evidence of an independent association with fat distribution. Whether the nature of the habitual diet and the degree of physical activity influence the incidence of NIDDM remains uncertain and should be further researched. Cardiovascular disease is strongly associated with NIDDM in most populations, but there are between-population differences in the degree of association and the relative excess in the two sexes. There is increasing evidence, in particular for coronary heart disease, that increased risk precedes the onset of hyperglycemia; the implication of this is that NIDDM and atherosclerosis share common antecedents. The specific complications of NIDDM--eye and renal disease--are important causes of morbidity and mortality and for those populations, often relatively poor, in which NIDDM is already or is becoming very common will pose substantial problems in provision of health care.
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PMID:Epidemiology and public health aspects of non-insulin-dependent diabetes mellitus. 268 May 53

A universal finding in hyperglycemic patients with type II (non-insulin-dependent) diabetes mellitus is that all share a common defect in glucose recognition resulting in abnormal insulin secretion by pancreatic islet beta-cells. This defect is 1) specific for glucose signals rather than global, 2) related to chronic hyperglycemia, and 3) partially reversible after brief treatment with insulin to induce normoglycemia and through use of other pharmacological agents without normalizing glucose levels. My perspective is that an essential component of this defect is secondary and may represent a state of homologous desensitization of the beta-cell secretory apparatus to glucose. Elucidation of the biochemical mechanism(s) of defective recognition of glucose signals by beta-cells--or glucose "non-sense"--in these patients will provide key insights into the pathogenesis of type II diabetes mellitus.
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PMID:Type II diabetes, glucose "non-sense," and islet desensitization. 268 9

This review summarized aspects of the widening scope, phenotypic expression, natural history, recognition, pathogeneses, and heterogenous nature of maturity-onset diabetes of the young (MODY), an autosomal dominant inherited subtype of NIDDM, which can be recognized at a young age. There are differences in metabolic, hormonal, and vascular abnormalities in different ethnic groups and even among Caucasian pedigrees. In MODY patients with low insulin responses, there is a delayed and decreased insulin and C-peptide secretory response to glucose from childhood or adolescence, even before glucose intolerance appears; it may represent the basic genetic defect. The nondiabetic siblings have had normal insulin responses for decades. The fasting hyperglycemia of some MODY has been treated successfully with sulfonylureas for more than 30 years. In a few, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they may resemble those of early Type I diabetes. The rate of progression of the insulin secretory defect over time does distinguish between these two types of diabetes. In contrast are patients from families who have very high insulin responses to glucose despite glucose intolerance and fasting hyperglycemia similar to those seen in patients with low insulin responses. In many of these patients, there is in vivo and in vitro evidence of insulin resistance. Whatever its mechanism, the compensatory insulin responses to nutrients must be insufficient to maintain normal carbohydrate tolerance. This suggests that diabetes occurs only in those patients who have an additional islet cell defect, i.e., insufficient beta cell reserve and secretory capacity. In a few MODY pedigrees with high insulin responses to glucose and lack of evidence of insulin resistance, an insulin is secreted which is a structurally abnormal, mutant insulin molecule that is biologically ineffective. No associations have been found between specific HLA antigens and MODY in Caucasian, black, and Asian pedigrees. Linkage studies of the insulin gene, the insulin receptor gene, the erythrocyte/Hep G2 glucose transporter locus, and the apolipoprotein B locus have shown no association with MODY. Vascular disease may be as prevalent as in conventional NIDDM. Because of autosomal dominant transmission and penetrance at a young age, MODY is a good model for further investigations of etiologic and pathogenetic factors in NIDDM, including the use of genetic linkage strategies to identify diabetogenic genes.
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PMID:Maturity-onset diabetes of the young (MODY). 268 21

In 12 members of a family with MODY, insulin and C-peptide release after intake of a test breakfast was measured as well as binding of insulin to its erythrocyte receptor. According to serum glucose concentrations, subjects were classified into: diabetic, carbohydrate intolerant, and normal subjects. The two diabetic patients had an insulin release pattern similar to that of non-insulin dependent diabetics. The two patients with carbohydrate intolerance presented hyperinsulinism either at base state and after stimulation. Of the eight normal subjects, three presented high concentrations of serum insulin either at base level and after stimulation; in the remaining five, base insulinemia was normal and the response after food intake was poor. Insulin binding to the receptor was decreased in diabetic patients and this anomaly was more evident in patients with carbohydrate intolerance. In the three patients with increased serum insulin concentration, no disturbances in insulin-receptor binding were detected; in the remaining five patients, insulin-receptor binding was significantly decreased. Our findings prove that these subjects present a disturbance of insulin release and an impairment of insulin-receptor binding with a predominance of one or the other alteration even before hyperglycemia is evident.
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PMID:[Insulin and peptide C secretion after food ingestion and the interaction of insulin with its erythrocyte receptor in a family with MODY type diabetes mellitus]. 269 74

Insulin clamp studies were carried out on 13 non-diabetics and 12 non-insulin-dependent diabetics (NIDDM). Based upon the body mass index (BMI), they were further divided into obese (BMI greater than or equal to 27 kg/m2) and nonbese groups (BMI less than 27 kg/m2). All received euglycemic insulin clamp study (Humulin-S 40mU/m2/min). Thermoregulated venous samplings were done every five minutes for measurements of plasma glucose (PG) and immunoreactive insulin (IRI). Steady state plasma glucose (SSPG) was obtained 20-80 minutes and kept for 100 more minutes. The data of final 40 minutes of clamp were used for analysis. Variations in SSPG and metabolic clearance rate of glucose (MCRG) instead of glucose infusion rate (M) value were used to assess the insulin sensitivity. The results showed that insulin resistance was noted in obese non-diabetic and diabetic subjects as well as in non-obese diabetic patients, as evidenced by higher basal IRI and lower MCRG than non-obese normal controls. Correlation analysis revealed that there was no correlation between the reduction of MCRG and the BMI in either non-diabetic or diabetic patients. There was a strong negative correlation between MCRG and the ambient fasting plasma glucose in the diabetic group, whereas this correlation was not found in the non-diabetic group. In conclusion, obesity with or without diabetes did have remarkable insulin resistance. In non-diabetic obese subjects the insulin resistance did not go up as the BMI increased further. In diabetic patients, both obesity and hyperglycemia contributed significantly insulin resistance.
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PMID:Insulin resistance in obesity and noninsulin dependent diabetes mellitus. 276 59

Little is known of the natural history of nephropathy in type 2 (non-insulin-dependent) diabetes, yet type 2 diabetes is a major cause of end-stage renal disease in the United States. The incidence rate of heavy proteinuria was determined in Pima Indians participating in a longitudinal population study of diabetes and its complications. Heavy proteinuria was defined by a urine protein (g/liter) to urine creatinine (g/liter) ratio greater than or equal to 1.0 (greater than or equal to 113 mg protein/nmol creatinine), a level which corresponds to a urine protein excretion rate of about 1 g/day. The incidence rates of proteinuria in diabetic Pimas were 4, 12, 37, and 106 cases/1,000 person-years at risk in the periods 0 to 5, 5 to 10, 10 to 15, and 15 to 20 years after the diagnosis of diabetes. The cumulative incidence rates were 2%, 8%, 23%, and 50% at 5, 10, 15, and 20 years, respectively. The duration of diabetes, severity of diabetes as determined by the degree of hyperglycemia and type of treatment, and blood pressure were risk factors for proteinuria. The presence of heavy proteinuria was strongly associated with the development of renal insufficiency, defined by serum creatinine greater than or equal to 2.0 mg/dl (greater than or equal to 177 mumol/liter). The incidence of proteinuria in type 2 diabetes in Pima Indians was as high as that reported in type 1 diabetes in other populations and represents a frequent, serious complication of the disease.
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PMID:Incidence of proteinuria in type 2 diabetes mellitus in the Pima Indians. 278 25

We studied the profile of nephropathy in 250 patients, 177 males and 73 females, with type 2 diabetes mellitus. The mean age was 55.9 +/- 8.8 years. Therapy for control of diabetes included diet alone in 1.6%, oral hypoglycaemic agents in 90.6% and insulin in 7.8%. Glycaemic control was satisfactory in 4.8%, fair in 41.2% and poor in 54.0%. Blood sugar values were normal without any therapy in 33 out of the 206 patients (16%) after the onset of renal insufficiency. The mean interval between the onset of diabetes and the appearance of proteinuria was 9.5 +/- 7.05 years. Proteinuria appeared within one year in 23 patients (9.2%), 1-5 years in 32 (12.8%), 6-10 years in 86 (34.4%) and more than 10 years in the remaining 109 patients (43.6%). Proteinuria was of nephrotic range in 17.6% of patients. Renal insufficiency was present in 206 (82.4%) patients and occurred 10.5 +/- 7.5 years after the detection of diabetes. Hypertension was present in 61.2% and was first detected 7.5 +/- 7.4 years after onset of diabetes. Endstage renal disease occurred 11.8 +/- 6.8 years after the onset of diabetes mellitus. Thus, clinical evidence of diabetic nephropathy is present in most patients with type 2 diabetes mellitus within a decade after the detection of diabetes. Subsequent progression to end-stage renal failure is rapid in the face of poorly controlled hypertension and hyperglycemia in the economically poor countries.
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PMID:Nephropathy in type 2 diabetes mellitus in Third World countries--Chandigarh study. 278 52

The use of dietary fiber (DF) in the diet of diabetics, although recommended, is often prevented by a limited tolerance and/or by the high cost and unpalatability of fiber supplements. Knowing that only or mainly the water soluble fraction of DF is effective in modulating postprandial hyperglycemia, the DF content (soluble, insoluble, and total) of a variety of common foodstuffs was determined. Such data were then utilized in the formulation of two complete meals, isocaloric and isoglucidic, characterized by a high-soluble, low-soluble, and total fiber content. The meals were administered to 13 NIDDM patients in good metabolic control. The data confirmed a significant reduction (p less than 0.001) of postprandial hyperglycemia and a moderate less significant reduction of insulinemia after the high fiber meal.
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PMID:Food fiber choices for diabetic diets. 282 13

Glycogen synthase (GS) catalyzes the formation of glycogen in human skeletal muscle, the tissue responsible for disposal of a significant portion of an oral carbohydrate load. Non-insulin-dependent diabetes mellitus (NIDDM) is characterized by fasting and postprandial hyperglycemia in conjunction with reduced rates of insulin-stimulated glucose disposal and storage in peripheral tissues, including muscle. Our objectives in this study were to determine whether ingestion of a mixed meal activates GS in control nondiabetic subjects and whether meal-related GS activation is reduced in NIDDM. To accomplish this, mixed formula meals were administered to 11 NIDDM and 9 age- and weight-matched nondiabetic control subjects. Plasma glucose and insulin values were measured before and for 90 min after meal ingestion. Skeletal muscle biopsies were performed just before and 90 min after meal ingestion for measurement of GS activity. Compared with control subjects, NIDDM subjects had significantly higher postprandial hyperglycemia and reduced postprandial hyperinsulinemia. GS was activated by meal ingestion in control subjects to a significantly greater extent than in NIDDM subjects. In NIDDM subjects, activation of GS was inversely correlated with fasting plasma glucose (r = .69, P less than .05). Therefore, NIDDM is characterized by reduced activation of a key step in the process of muscle glycogen repletion after a meal. Reduced activation of GS by a mixed meal in NIDDM may contribute to the reduced glucose disposal after a meal, thus contributing to the hyperglycemia observed in these subjects.
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PMID:Decreased activation of skeletal muscle glycogen synthase by mixed-meal ingestion in NIDDM. 283 18


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