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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of non-infective skin associations of diabetes mellitus was conducted on 100 consecutive outpatient diabetics over a 3-month period. 10 were insulin-dependent diabetics (IDDM), 24 insulin-requiring and 66 non-insulin dependent diabetics (NIDDM). A total skin evaluation was done for each patient with skin biopsy whenever appropriate. Twenty-three patients had diabetic dermopathy; the frequency of retinopathy in this group (39.1%) is significantly higher than that without diabetic dermopathy (6.9%) (p less than 0.001). There were 20 instances of cutaneous complications of therapy; 10 had insulin lipodystrophy (29.4% of 34 insulin users). Twelve patients, 8 of whom were overweight, had acanthosis nigricans. There were 6 Indians among them and all the patients had NIDDM. Eight had xanthelasma. Vitiligo occurred in 3.3% of those with NIDDM. Classical scleredema diabeticorum and cheiroarthropathy occurred in 2% of patients. One patient had atypical granuloma annulare. There was a higher incidence of xanthelasma in our study compared with studies done previously. Insulin lipodystrophy and acanthosis nigricans in the absence of classically described syndromes of insulin resistance seem to be fairly common phenomena and merit further investigation locally.
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PMID:Non-infective skin associations of diabetes mellitus. 322 40

We have reviewed the role of insulin in ovarian physiology. Clinical observations and experimental data strongly support the hypothesis that insulin possesses gonadotropic activity, when acting alone or with FSH or LH. This idea is further supported by the recent discovery of insulin in follicular fluid. The idea that insulin has gonadotropic function can explain a variety of clinical observations, which otherwise are difficult to understand. For example, manifestations of ovarian hypofunction (primary amenorrhea, late menarche, anovulation, low pregnancy rate, and early menopause) in IDDM can be understood if it is accepted that insulin is necessary for the ovary to reach its full steroidogenic potential. The idea that insulin affects ovarian steroidogenesis also helps to understand the observation that hyperandrogenism frequently accompanies each of the various insulin-resistant states, regardless of the latter's etiology (e.g. genetic deficiency in the number of insulin receptors, antiinsulin receptor antibodies, obesity, etc.). The explanation for this association is based on the idea that hyperinsulinemia intensifies ovarian steroidogenesis, which manifests clinically as hyperandrogenism. Continuous stimulation of the ovary by insulin over a long period of time possibly produces morphological ovarian changes, such as hyperthecosis or polycystic changes; these changes commonly are observed among women with insulin resistance. The effects of insulin on ovarian cells are mediated possibly through binding of the peptide to its own receptor or to the IGF-1 receptor (the specificity spillover phenomenon). The latter could be an important mechanism in cases of insulin resistance. Potential mechanisms underlying the gonadotropic activity of insulin include direct effects on steroidogenic enzymes, modulation of FSH or LH receptor number, synergism with FSH or LH, or nonspecific enhancement of cell viability. The gonadotropic function of insulin adds yet another note to what has been termed a symphony of insulin action. Further investigation into this new area may yield greater insights not only into normal ovarian physiology, but also into the pathogeneses of such diverse entities as PCO, obesity, diabetes mellitus, and the syndromes of insulin resistance and acanthosis nigricans.
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PMID:The gonadotropic function of insulin. 330 17

New dimensions have been acquired in the physiopathology of insulin-resistant syndromes, by measurement of insulin receptors and advances in knowledge of their structure and function. The insulin-resistance of obese subjects and non-insulin dependent diabetics is related to both a reduction in the number of receptors, responsible for diminished sensitivity to insulin, and alterations in the action of the hormone at the post-receptor stage, with resulting suppression of the maximal response to insulin. The number of receptors varies as a function of blood insulin levels, hyperinsulinism being associated with a reduction in their number (negative feed-back). Post-receptor stages appear to be particularly sensitive to either absolute (insulin-dependent diabetes) or relative (non-insulin dependent diabetes) insulinopenia. The rare syndromes of extreme insulin resistance, often accompanied by acanthosis nigricans, represent a heterogeneous collection divisible into 3 sub-groups. In type A there is reduced insulin binding related to a possible primary anomaly (genetic) of the receptor. Type B is characterized by the presence of serum auto-antibodies directed against the receptor, while in type C the anomalies exist at the post-receptor stage. Insulin accelerates degradation of its specific receptor, a mechanism capable of explaining (at least partly) the negative feed-back control of the receptor by the hormone. The insulin-receptor complexes undergo intracellular transfer and a return to the plasmic membrane, but possible physiopathological implications of this movement have not been established. The receptor includes two principal glycoprotein subunits; alpha (130 kilodaltons) and beta (95 kilodaltons).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Insulin resistance. Physiopathological and biochemical aspects]. 639 63

Differentiating NIDDM-Y from IDDM in youth is a diagnostic challenge. Serum insulin levels at diagnosis may help differentiate between NIDDM-Y and IDDM if the level is elevated, but the serum insulin level is low or undetectable in 45% of patients with NIDDM-Y. Islet-specific antibodies may be present in serum at diagnosis, and ketosis or ketoacidosis may occur. For our patients, clinical features are most helpful in differentiating NIDDM-Y from IDDM and include ethnic background, age and gender at diagnosis (approximately 80% of First Nation patients from northern Manitoba are adolescent females), presence of obesity and acanthosis nigricans, lack of symptoms or weight loss, and strong family history of NIDDM.
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PMID:Diagnostic criteria for non-insulin dependent diabetes in youth (NIDDM-Y). 949 13

Data are presented comparing non-insulin dependent diabetes mellitus (NIDDM) and insulin dependent diabetes mellitus (IDDM) in youth. Children and adolescents with NIDDM were predominantly Mexican-American, presented less frequently in ketoacidosis, had a greater frequency of family history of diabetes, had higher BMIs (27.4 vs 16.6 kg/m2), and had higher frequency of acanthosis nigricans (67% vs 1.2%). Logistical, social, and cultural challenges facing the physician treating children and adolescents with NIDDM are discussed, and treatment options for NIDDM in youth are briefly reviewed.
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PMID:Non-insulin dependent diabetes in children and adolescents: the therapeutic challenge. 949 18

We report on a 33-year-old male patient with generalized acquired lipodystrophy, insulin resistant diabetes mellitus and acanthosis nigricans (Lawrence Syndrome). First probable symptoms of lipodystrophy (weight loss, shrinkage of subcutaneous fatty tissue, and loss of muscular strength) became evident three years ago, with the onset of diabetes mellitus occurring about six months later. The patient suffered from the following clinical symptoms: IDDM with increasing insulin-requirement, extreme reduction of fatty tissue, fatty liver hepatitis with elevated liver enzymes, glomerulopathy, muscular and neuropathic pains, as well as hypertriglyceridaemia. A basal C-peptide concentration is rather high. Definitely, the endogenous insulin secretion is increased. In other words, insulin resistance is documented. In an effort to identify the pathogenetic mechanisms of lipoatrophic diabetes mellitus in this patient and to develop a therapeutic strategy, antibodies against different tissues and endocrinologic regulation were investigated. It was possible to demonstrate the presence of serum autoantibodies against lipocytes of the subcutis and other tissues, against hepatic stellate cells, together with autoantibodies against different endocrine organs. By studying the basis of diabetic abnormalities relating to the growth hormone (GH), the insulin-like growth factor (IGF) dynamics in this patient, i.e. reductions of GH, IGF-I, IGF-II, IGF-Binding protein (IGF-BP) 2 and IGF-BP 3, were detected. An immunosuppressive treatment strategy was not beneficial.
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PMID:Dysregulation of insulin-like growth factors in a case of generalized acquired lipoatrophic diabetes mellitus (Lawrence Syndrome) connected with autoantibodies against adipocyte membranes. 951 65

PURPOSE: To contrast incidence rates and time trends of typical type 1 diabetes with non-autoimmune insulin-resistant type 2 diabetes in minority children (Early 2).METHODS: A population based registry of all insulin treated African-American and Hispanic children residing in Chicago, aged 0-17 years at onset, diagnosed between 1985-1994 provided data. Medical records were reviewed and abstracted (N = 739), and a subset of patients were interviewed (n = 195). Based on these data sources, cases were assigned to the early type 2 category if one or more of the following variables were present: notation of "atypical" or "possible type 2" diabetes in the medical record; obesity (defined as BMI >/= 27 (kg/m(2))) or acanthosis nigricans noted at diagnosis; a report by the patient of going off insulin six months after initial diagnosis without developing diabetic ketoacidosis; or reporting the use of oral hypoglycemic agents with or without insulin. The Chi-square test for homogeneity was used to determine differences between proportions of groups. Time trend analysis of incidence was done using regression models with the Poisson distribution.RESULTS: The 10-year average annual incidence rate was 10.3 per 100,000 population for typical type 1 diabetes (n = 565) and 3.2 per 100,000 for those with characteristics of early 2 diabetes (n = 174). Over the ten year interval the incidence rate remained static for typical type 1 diabetes. In the early 2 group there was a 9.0% average annual percent increase over the ten year interval (p < 0.01).CONCLUSIONS: The trends in incidence rates vary between typical type and early 2 diabetes. We hypothesize that this is associated with the increasing rate of obesity and a lack of physical activity in young people.
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PMID:Are trends in diabetes incidence changing for minority children? 1101 69

Autoantibody and T cells reacting with islet proteins have been demonstrated in patients with type 1 diabetes. In recent years an increasing number of children have been clinically classified with type 2 (not ketosis prone, evidence of insulin resistance, presence of acanthosis nigricans, and obesity) or indeterminant diabetes (admixture of clinical features of types 1 and 2). In this study, we compared the islet cell autoantibody and T-cell responses to islet proteins in type 2 (n = 19) and indeterminant (n = 16) children (<18 yr of age) to classic type 1 (n = 37) diabetic patients. We observed that 37 of 37 type 1 diabetic children demonstrated autoantibody and/or T-cell reactivity to islet proteins. Fourteen of the 19 type 2 patients were positive for islet cell autoantibodies, and six of 14 were positive for T-cell responses to islet proteins. For the indeterminant patients, 11 of 16 of the patients were positive for autoantibodies, and six of 16 patients were positive for T-cell responses to islet proteins. These results demonstrate that autoimmunity to islet proteins is present in a high percentage of children classified as indeterminant or type 2 diabetes. Moreover, the presence of obesity or acanthosis nigracans does not reliably distinguish children with or without islet cell autoimmunity.
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PMID:Autoimmunity to islet proteins in children diagnosed with new-onset diabetes. 1512 45

There has been wide recognition in the past decade of the increasing frequency of type 2 diabetes in youth, largely but not exclusively in North America. In some American locations and populations, incidence and prevalence of type 2 diabetes are much higher than those of type 1 diabetes, because of increased calorie and fat intake, and decreased exercise. The increasing prevalence of type 2 diabetes in the United States has closely paralleled the increase in childhood obesity noted there, but now across the Western world. Besides obesity, the other youth risk factors for type 2 diabetes are: ethnicity, puberty, family history, metabolic syndrome, polycystic ovary syndrome, acanthosis nigricans. Any feature or condition associated with insulin resistance/hyperinsulinemia should alert to screen youth at increased risk for (pre)type 2 diabetes. Treatment goals are to decrease weight and increase exercise, to normalize insulinemia, glycemia and HbA1c, to control hypertension and hyperlipidemia. The aim of the pharmacological therapy is to decrease insulin resistance, namely by metformin. Sometimes, insulin therapy is necessary.
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PMID:[Weight of obesity in (pre)type 2 diabetes in children and adolescents: how and when to screen for?]. 1628 80

Type 2 diabetes (T2DM) is now a pediatric disease. As in adults, it disproportionately affects ethnic and racial minorities, including Hispanics. The preponderance of Hispanics in south Texas are of Mexican American (MA) heritage. Over the past 16 years, we have accumulated a large cohort of children with diabetes. We have noted distinct differences in numerous parameters between MA children with T2DM and those with type 1 diabetes (T1DM). In order to explore these observations, we have reviewed the records of all children diagnosed with diabetes (n = 669) during the 9 years between January, 1990 and December, 1998 and seen by our pediatric diabetes group. In this cohort were 329 MA, 287 non-Hispanic whites (EA) and 53 African Americans. Compared to EA children with T1DM, MA children were more likely to have a parent with diabetes, to be hospitalized at the time of diagnosis and to lack health insurance. The differences between MA children with T1DM and T2DM were significant: specifically, children with T2DM were more likely to be female and pubertal with a body mass index >25 kg/m(2) and have acanthosis nigricans. Slightly more than 2/3 of the MA children with T2DM had at least one parent already diagnosed with T2DM. Less than 1/3 of the children with T2DM required hospitalization at the time of diagnosis and only a 1/4 have private health insurance. Over this 9-year interval, the apparent incidence of diabetes almost tripled in south Texas with the great majority of that increase due to the increasing numbers of children with T2DM.
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PMID:The changing spectrum of diabetes in Mexican American youth. 1719 13


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