Active Sense: Early Staging of Non-Insulin Dependent Diabetes Mellitus (NIDDM) Hinges upon Recognizing Daily Activity Pattern

The Human Activity Recognition (HAR) system allows various accessible entries for the early diagnosis of Diabetes as one of the nescient applications domains for the HAR. Long Short-Term Memory (LSTM) was applied and recognized 13 activities that resemble diabetes symptoms. Afterward, risk factor assessment for an experimental subject identified similar activity pattern attributes between diabetic patients and the experimental subject. Because of this, a trained LSTM model was deployed to monitor the average time length for every activity performed by the experimental subject for 30 consecutive days. Concurrently, the symptomatic diabetes activity patterns of diabetic patients were explored. The cosine similarity of activity patterns of the experimental subject and diabetic patients measured 57.39%, putting the experimental subject into moderate risk factor class. The experimental subject was clinically tested for risk factors using the diabetic clinical diagnosis process, known as the A1C. The A1C level was 6.1%, recognizing the experimental subject as a patient suffering from Diabetes. Thus, the proposed novel approach remarkably classifies the risk factor level based on activity patterns.

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Hepatic drug metabolism is increased in poorly controlled insulin-dependent diabetes mellitus

Acta Endocrinologica ◽

10.1530/acta.0.1230550 ◽

1990 ◽

Vol 123 (5) ◽

pp. 550-556 ◽

Cited By ~ 15

Author(s):

Steven Goldstein ◽

Anna Simpson ◽

Paul Saenger

Keyword(s):

Diabetes Mellitus ◽

Insulin Dependent Diabetes Mellitus ◽

Diabetic Control ◽

Insulin Dependent Diabetes ◽

Dependent Diabetes Mellitus ◽

Diabetic Patients ◽

Hepatic Drug Metabolism ◽

Hepatic Drug ◽

Insulin Dependent ◽

Cytochrome P 450

Abstract. In addition to increased glycosylation of hemoglobin, abnormalities of other heme proteins such as cytochrome P-450 might also occur in patients with insulin-dependent diabetes mellitus. Antipyrine is a useful marker drug for cytochrome P-450 dependent hepatic drug metabolism. Antipyrine kinetics and urinary excretion of antipyrine metabolites were measured in 14 patients with insulin-dependent diabetes mellitus in poor metabolic control. Improvement in diabetic control in 9 patients, as measured by more normal HbA1 values, led to normalization of plasma antipyrine half-time (t½) and metabolism: the mean antipyrine t½ slowed from 4.7±0.2 (sem) initially to 7.8±0.3 h in these 9 patients and was thus nearly identical to that of normal subjects 8.6±1.0. Antipyrine plasma clearance improved in the 9 diabetic patients whose diabetic control improved. The apparent volume of distribution was normal on both occasions in the diabetic patients. These findings provide a new argument for tight metabolic control in patients with insulin-dependent diabetes mellitus.

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FTIR Spectroscopic Investigation of Mineral Structure of Streptozotocin Induced Diabetic Rat Femur and Tibia

Spectroscopy An International Journal ◽

10.1155/2003/826545 ◽

2003 ◽

Vol 17 (2-3) ◽

pp. 627-633 ◽

Cited By ~ 11

Author(s):

Handan Boyar ◽

Belma Turan ◽

Feride Severcan

Keyword(s):

Diabetes Mellitus ◽

Insulin Dependent Diabetes Mellitus ◽

Insulin Dependent Diabetes ◽

Dependent Diabetes Mellitus ◽

Diabetic Rat ◽

Carbonate Content ◽

Diabetic Patients ◽

Type I ◽

Mineral Density ◽

Insulin Dependent

Diabetes mellitus (DM) can be accepted as a heterogenous multi organ disorder that can affect various systems of the human body. Disorders include retinopathy, neuropathy, cardiomyopathy, musculoskeletal abnormalities such as diminished bone formation and bone healing retardation. Low bone mineral density is often mentioned as a complication for patients with insulin dependent diabetes mellitus (type I DM). Streptozotocin (STZ) induced diabetic rats are good models for investigation of the complications of insulin dependent diabetes. In the present study, the effects of STZ induced diabetes on the mineral environment of rat bones namely femur and tibia were studied by Fourier transform infrared (FTIR) spectroscopic technique. The results revealed that mineral crystal sizes increased and carbonate content decreased for diabetic femur and tibia. These changes can be due to the formation of osteoporosis which is widely seen in diabetic patients.

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Diabetic Ketoacidosis in Children and the Role of Outpatient Management

Pediatrics in Review ◽

10.1542/pir.11.10.297 ◽

1990 ◽

Vol 11 (10) ◽

pp. 297-304 ◽

Cited By ~ 1

Author(s):

H. Peter Chase ◽

Satish K. Garg ◽

David H. Jelley

Keyword(s):

Diabetic Ketoacidosis ◽

Hospital Admissions ◽

Insulin Dependent Diabetes Mellitus ◽

The United States ◽

Absolute Number ◽

Dependent Diabetes Mellitus ◽

National Commission ◽

Diabetic Patients ◽

Intravenous Insulin ◽

Insulin Dependent

Diabetic ketoacidosis (DKA) is a common complication among children with diabetes, accounting for 14% to 31% of all diabetes-related hospital admissions.1,2 Extrapolation of data from the National Commission on Diabetes3 suggests that there are approximately 160 000 admissions to private hospitals each year in the United States for DKA. The cost of hospitalizations for DKA is over one billion dollars annually. Sixty-five percent of all patients admitted are less than 19 years of age. The incidence of DKA is believed to be declining. However, because the numbers of subjects with insulin-dependent diabetes mellitus is increasing, the absolute number of hospitalizations for DKA is still increasing. It is the single most common cause of death in diabetic patients under 24 years of age.2 The treatment of DKA has changed in recent years, particularly with the use of low-dose continuous intravenous insulin infusion and with the availability of blood pH levels. Severe DKA has been defined as "a state of ketoacidosis with serum bicarbonate decreased to 10 mmol/L or less," or more recently, as a "pH of 7.1 or less."4 The mortality from DKA has been reported to be in the range of 0.5 to 15.4%.3,5 Previous mortality figures were as high as 38%.2

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Dissociation of in vitro sensitivities of glucose transport and antilipolysis to insulin in NIDDM

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1987.253.3.e300 ◽

1987 ◽

Vol 253 (3) ◽

pp. E300-E304 ◽

Cited By ~ 3

Author(s):

H. Yki-Jarvinen ◽

K. Kubo ◽

J. Zawadzki ◽

S. Lillioja ◽

A. Young ◽

...

Keyword(s):

Insulin Resistance ◽

Glucose Transport ◽

American Indians ◽

Insulin Dependent Diabetes Mellitus ◽

Insulin Binding ◽

Dependent Diabetes Mellitus ◽

Diabetic Patients ◽

Insulin Dependent ◽

Obese Subjects

It is unclear from previous studies whether qualitative or only quantitative differences exist in insulin action in adipocytes obtained from obese subjects with non-insulin-dependent diabetes mellitus (NIDDM) when compared with equally obese nondiabetic subjects. In addition, the role of changes in insulin binding as a cause of insulin resistance in NIDDM is still controversial. We compared the sensitivities of glucose transport and antilipolysis to insulin and measured insulin binding in abdominal adipocytes obtained from 45 obese nondiabetic (% fat, 41 +/- 1), 25 obese diabetic (% fat, 40 +/- 1), and 15 nonobese (% fat, 30 +/- 1) female southwestern American Indians. Compared with the nonobese group, the sensitivities of glucose transport and antilipolysis were reduced in both the obese nondiabetic and obese diabetic groups. Compared with the obese nondiabetic subjects, the ED50 for stimulation of glucose transport was higher in the obese patients with NIDDM (171 +/- 38 vs. 92 +/- 10 pM, P less than 0.005). In contrast, the ED50s for antilipolysis were similar in obese diabetic patients (32 +/- 6 pM) and obese nondiabetic subjects (27 +/- 3 pM). No difference was found in insulin binding in patients with NIDDM when compared with the equally obese nondiabetic subjects. These data indicate 1) the mechanism of insulin resistance differs in NIDDM and obesity, and 2) the selective loss of insulin sensitivity in NIDDM precludes changes in insulin binding as a cause of insulin resistance in this disorder.

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