Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The islets of Langerhans provide energy storage and disposal, and protection from plasma glucose excursions, especially hypoglycemia. Insulin-dependent diabetes mellitus (IDDM) results from autoimmune beta-cell damage. Prevention of IDDM has already been achieved in animal investigation and some centers are now screening and treating individuals at high risk for developing IDDM. Immunosuppressive drugs can induce transient remission of recent-onset IDDM. Intensive insulin treatment of IDDM delays the onset and slows the progression of long-term complications. Non-insulin dependent diabetes mellitus (NIDDM) is the result of beta-cell malfunction and is strongly associated with X syndrome. Diet and exercise are of undoubted importance in NIDDM prevention and treatment. Functional endocrine tumors of the pancreas (FET) are rare hormone and peptide-secreting neoplasms. These peptides may or may not occur naturally in the islets. FETs often occur with multiple endocrine neoplasia 1 (MEN 1) so that MEN-1 screening should always be performed, and extended to family members whenever diagnosed. Drugs--alcohol, insulin and sulfonilureas--are the main cause of hypoglycemia. Insulinoma is the main cause of post-absorptive organic hypoglycemia. Non islet-cell tumors seldom cause hypoglycemia. Insulinoma often is a solitary tumor, but it may be multicentric and may coexist with cell hyperplasia and nesidioblastosis. Symptoms of neuroglycopenia may be mistaken for neuropsychiatric disease. The diagnosis is based on confirmation of post absorptive hypoglycemia and hyperinsulinism. Gastrinoma causes Zollinger-Ellison syndrome (ZES) which is characterized by fulminating peptic ulcer disease. The tumor is often malignant, and it may be multicentric and may occur with cell hyperplasia and nesidioblastosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The endocrine pancreas]. 765 6

Hispanic elders living in the United States compose a rapidly increasing population. They are underinsured and more likely to be living in poverty. Health care is hindered in this population by lower access to health services and less use of preventive services. Barriers to access are primarily socioeconomic. Acculturation exerts an effect, primarily through its association with language skills, employment, and education. Cardiovascular disease is the leading cause of mortality for Hispanics, who have a higher prevalence of risk factors for cardiovascular disease, such as diabetes mellitus, obesity, and hyperlipidemia. Although neoplasia is the second most frequent cause of death among Hispanics, as it is in whites who are not Hispanic, Hispanics have an overall lower cancer rate. Cancer rates are increasing, however. Non-insulin-dependent diabetes mellitus is a significant cause of morbidity and mortality in the Hispanic population, affecting nearly a quarter of adult Puerto Ricans and Mexican Americans. Although higher prevalence of obesity in the Hispanic population accounts for some of this difference, some data suggest the possibility of a genetic component as well. Assessment of psychological health in Hispanic elders is impeded by the lack of instruments designed for this population. Distress is often expressed as somatic symptoms. Values traditional to Hispanic culture, such as respeto, allocentrism, and familialism, are important to US Hispanic elders, many of whom were born in rural Mexico. Our knowledge of determinants of healthy aging in this population is still preliminary, but rapidly expanding, in part, because of increased attention to ethnicity in health reporting.
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PMID:Health status of Hispanic elders. 772 19

Advances in molecular biology techniques suggest that many haematological neoplasms originate from a transformation process at the level of the haemopoietic pluripotential stem cell. While familial aggregation has been reported for many haematological neoplasms, most studies were uncontrolled and examined the presence of the same haematological neoplasm as the index case. We assessed the familial aggregation of all haematological neoplasms in 4061 family members of 189 patients with various haematological neoplasms and two control groups: 955 relatives of 36 patients with non-malignant haematological disorders and 508 relatives of 33 patients with type II diabetes mellitus. Data collection included self-administered questionnaires. The odds ratio for haematological neoplasms among relatives of the index cases adjusted for age, sex, ethnicity, number of relatives in the family, and degree of familial linkage in the study group versus the two control groups was 3.62 (95% confidence interval, 1.44-9.07; P < 0.01). The vast majority of the haematological neoplasms among family members did not belong to the same histopathological category as the index cases. The data support the hypothesis of a genetic predisposition to haematological neoplasms. The fact that the aggregation is not disease specific is consistent with a defect in the pluripotent haemopoietic stem cell.
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PMID:Familial aggregation of haematological neoplasms: a controlled study. 794 58

To evaluate beta-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type II diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type II diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type II diabetics. It is concluded that the altered beta-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
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PMID:Beta-cell function in pancreatic adenocarcinoma. 802 55

This study determined the effects of exercise on the ability of inflammatory macrophages to inhibit tumor cell growth in vitro (macrophage cytotoxicity). Thioglycollate injection (1 ml ip) was used as an inflammatory challenge and to partially activate macrophages for cytotoxicity. Inbred male C3H/HeN mice (n = 180) exercised moderately (MOD, 18 m/min, 30 min/day, 5% grade) or to exhaustion (EXH, 18-35 m/min, 2-4 h, 5% grade) on a motor-driven treadmill for 3 consecutive days after injection. Control (CON) mice were kept in stimulated treadmill lanes directly over the runners. Mice were killed immediately or 3 or 8 h postexercise. Macrophages from both MOD and EXH exercise groups manifested significantly (P < 0.05) enhanced (approximately 50%) cytotoxicity compared with those from CON group at all time points postexercise. This potentially beneficial exercise effect was not related to macrophage production of interleukin-1 beta, reactive nitrogen or oxygen intermediates, or number of macrophages in the assay but may have been manifested, in part, by tumor necrosis factor-alpha. Plasma corticosterone was significantly elevated immediately postexercise in MOD and EXH compared with CON mice; however, no evidence existed for an immuno-suppressive effect of corticosterone on macrophage cytotoxicity, perhaps because of insensitivity of inflammatory macrophages to glucocorticoid suppression seen in vitro. These data only partially support the "inverted U hypothesis," which states that moderate exercise may enhance, whereas very heavy exercise or a lack of exercise may attenuate, the immune response. Further study is needed to determine the physiological significance of these findings and the effects of exercise on macrophage subsets sensitive to glucocorticoid suppression (i.e., fully activated macrophages).
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PMID:Exercise increases inflammatory macrophage antitumor cytotoxicity. 822 94

Partial ophthalmoplegia due to third nerve palsy with an intact pupil is a frequent cause of diploplia observed in diabetic patients. Pupillary muscle involvement, such as anisocoria and loss of light reflex, is usually uncommon in this diabetic cranial mononeuropathy. A 65-year-old woman with non-insulin dependent diabetes mellitus (NIDDM) suddenly developed a severe headache and diplopla. Right oculomotor nerve palsy was observed in association with anisocoria, ptosis of the right lid, and a defective light reflex. No exophthalmos or vascular bruit was observed in the right orbital region. Computed tomography and magnetic resonance images of the head were negative. Cerebral angiography revealed a carotid cavernous sinus fistula (CCF). The patient was successfully treated with external carotid artery embolization combined with radiation. It is well known that pupil sparing in oculomotor nerve palsy predicts an extraaxial ischemic lesion, while pupil involvement predicts an extraaxial compression lesion. Therefore, pupillary involvement in oculomotor nerve palsy in diabetic patients necessitates cerebrovascular investigation to rule out ICPC aneurysm or tumor. In this circumstance, a variant type of CCF without characteristic ocular signs should be included in the differential diagnosis.
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PMID:[A case of NIDDM associated with oculomotor palsy due to atypical carotid cavernous sinus fistula]. 827 44

Metastases of breast cancer are a major cause of treatment failure. To evaluate the therapeutic efficacy of suicide gene therapy in metastatic breast cancer, we used the herpes simplex virus thymidine kinase (HSV-tk) gene followed by ganciclovir (GCV) administration to treat breast cancer, generated by an adenocarcinoma cell line MOD in syngeneic mice. The bystander effect of HSV-tk + GCV on tumor cell killing was illustrated by demonstrating complete regression of subcutaneous tumors consisting of 90% parental tumor cells and 10% HSV-tk transformed tumor cells. To establish a model of breast cancer metastases in the liver, tumors were generated by intra-hepatic implantation of MOD cells in syngeneic animals. Two weeks after tumor cell implantation, replication defective adenoviral vectors expressing HSV-tk (ADV.tk), or beta-galactosidease (ADV. beta-Gal) were injected intratumorally, followed by buffer or GCV administration. Treatment with ADV.tk + GCV resulted in significant regression of tumor (P < .001), as assessed by computerized morphometric analysis of residual tumor. This was reflected as a significant prolongation of survival in treated animals (P < .001). These results demonstrate that ADV-mediated suicide gene therapy in vivo can be incorporated in a comprehensive treatment strategy for liver metastases of breast cancer.
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PMID:Adenoviral-mediated suicide gene therapy for hepatic metastases of breast cancer. 889 53

Hyperandrogenism is characterized clinically by hirsutism, acne, androgens-dependent alopecia and elevated serum concentrations of androgens (testosterone and androstenedione). Polycystic ovary syndrome is the most frequent cause of hyperandrogenism. Nevertheless, the differential diagnosis includes androgen-secreting tumors of the ovary or adrenal gland. Although rare, it is important to consider this diagnosis in patients with serum testosterone concentrations greater than 7 nmol/l. A 35-year-old woman who presented with hirsutism, amenorrhea and acanthosis nigricans is described. The endocrine abnormalities included a serum testosterone concentration of 9 nmol/l and overt type II diabetes mellitus. Imaging studies, including magnetic resonance imaging and Doppler ultrasonography, did not disclose a secreting tumor. After cyproterone acetate was prescribed the serum testosterone concentration returned to normal. The recent application of modern, high-resolution diagnostic ultrasonography and magnetic resonance imaging enabled a morphologically based diagnosis in a case of severe hyperandrogenism, with no need for invasive procedures. The therapeutic response to antiandrogens is reassuring.
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PMID:A case of severe hyperandrogenism, acanthosis nigricans and over diabetes: the use of non-invasive methods for diagnosis, pathogenesis and management. 891 63

Recent evidence suggests that insulin is mitogenic on the adrenal cortex and stimulates adrenocortical tumor formation. We, investigated whether hyperinsulinemia is present in 13 patients with incidentally detected adrenal tumors. Patients with adrenal incidentalomas were obese (mean BMI 29.7 +/- 1.2 kg/m2, normal < 25; % body fat 35 +/- 1.5%, normal < 30%) with increased abdominal fat deposition (waist to hip ratio 0.92 +/- 0.02, normal < 0.85). All 13 patients were insulin resistant. Five had NIDDM, of the remaining patients 5 had fasting insulin concentrations above 15 microE/ml, and all 8 patients had elevated insulin concentrations after 75 g of glucose orally. To further investigate the potential role of insulin we examined its effects on the NCI-h295 cell line. Insulin (1-100 micrograms/ml) stimulated cell proliferation in a time and dose-dependent matter without affecting cortisol synthesis. At this concentrations insulin was equally potent to IGF I (10-80 ng/ml) or IGF II (10-100 ng/ml). We conclude that the majority of patients with adrenal incidentalomas are insulin-resistant/hyperinsulinemic. Insulin stimulates adrenal cancer cell lines in vitro. We propose that adrenal incidentalomas are a newly recognized manifestation of the metabolic syndrome comparable to insulin-mediated stimulation of the ovary in the polycystic ovary syndrome.
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PMID:Adrenal incidentalomas: a manifestation of the metabolic syndrome? 896 38

Recent sibling-pair linkage analyses have indicated possible linkage of noninsulin dependent diabetes mellitus (NIDDM) with a number of markers on the long arm of chromosome 7. A coincidental and recent discovery is that specific genetic anomalies identified on chromosome 7 in uterine leiomyoma tumor cells in many cases correspond, cytogenetically, to the same region where genetic linkage to insulin resistance has been identified. In the present study, 15 closely spaced microsatellite markers were used to finely map deletion breakpoints and to test for allelic loss of 7q markers in 12 uterine leiomyoma tumor samples with cytogenetically defined deletions. Of the 9 informative tumor samples, three exhibited breakpoints in the same region where genetic linkage to insulin resistance has been identified (between PON and UT901). Because breakpoints in neoplasias often occur within or adjacent to expressed sequences, these breakpoints may provide a molecular tool to aid in the identification of candidate genes for insulin resistance.
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PMID:Molecular analysis of chromosome 7q21.3 in uterine leiomyoma: analysis using markers with linkage to insulin resistance. 942 63


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