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Diabetes Mellitus, Obesity, Lipoprotein Disorders and other Metabolic Diseases
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
A number of gene mutations with a high penetrance and large effect on glucose metabolism can be thought of as monogenic forms of diabetes. The best described group is MODY (‘maturity onset diabetes of the young’). These patients have a phenotype like type 2 diabetes (mild hyperglycaemia without ketosis) but are not obese and the onset of their diabetes is usually before the age of 25 years with autosomal dominant inheritance (Table 11.2).
Endocrinology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Mehul Dattani, Catherine Peters
In addition to the diagnostic glucose and HbA1c concentrations, a urine dipstick test for ketonuria should also be undertaken. Absence of ketonuria might indicate type 2 diabetes or maturity onset diabetes of the young (MODY). Markers of the process of immune-mediated destruction are present in 85–98% of children with newly diagnosed type 1 diabetes. These include autoantibodies to insulin (IAA), autoantibodies to glutamic acid decarboxylase (GAD65) and autoantibodies to the tyrosine phosphatases IA-2 and IA-2β.
ANTIDIABETIC ACTIVITY OF Hypericum mysorense Heyne
Published in V. R. Mohan, A. Doss, P. S. Tresina, Ethnomedicinal Plants with Therapeutic Properties, 2019
V. Sornalakshmi, P. S. Tresina, K. Paulpriya, V. R. Mohan
Juvenile DM: Among several monogenic forms of DM which have been identified, maturity onset diabetes of the young (MODY) is a familial form of NIDDM with autosomal dominant inheritance, which usually develops in childhood, adolescence, or young adulthood, and presents primarily insulin secretion defects (Raffel et al., 1997). MODY is not a single entity, but involves genetic, metabolic, and clinical heterogeneity. Mutations in six genes cause most cases of MODY (MODY 1–MODY 6) (Horikawa et al., 1997; Malecki et al., 1999). The prevalence of MODY is unknown but about 2–5% of patients with type 2 diabetes may in fact have MODY (Lederman, 1995). The term juvenile onset diabetes has sometimes been used for IDDM and maturity onset for NIDDM (Bastaki, 2005).
Islet hypoplasia of adult offspring rats caused by intrauterine chronic hypoxia is compensated by up-regulation of INS and PDX-1
Published in Islets, 2023
Tianfeng Chen, Yang Xiao, Shaodan Xu, Helin Ke, Shilin Li
In our study, adult male islets in the offspring of the ICH group had reduced islet area and β-cell number compared to those in the NC group. These results suggest that β-cells are damaged functionally and that damaged β-cells may initiate apoptosis, further reducing the number of β-cells. At present, there are mainly two theories,25–27 constant endoplasmic reticulum stress and glucolipotoxicity effect, which suggest that after the damage of β-cells, the apoptosis process is initiated, causing a large number of β-cells to decrease. Our results are consistent with previous studies. In addition, the decreased positive cell area of INS and GLUT2 was further evidence of the decrease of β-cells. Because studies have shown that in maturity-onset diabetes of the young type 3 (MODY3) patients, downregulated GLUT2 levels and mutations in the encoding gene SLC2A2 cause a defect in INS secretion.28
The role of sulfonylureas in the treatment of type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2022
Brian Tomlinson, Nivritti Gajanan Patil, Manson Fok, Paul Chan, Christopher Wai Kei Lam
Maturity-onset diabetes of the young (MODY) due to dominant mutations in one of at least 13 different genes occurs in <5% of people with diabetes and usually manifests before the age of 25 years [116,117]. MODY3 caused by mutations in the gene for hepatocyte nuclear factor 1 α (HNF1A) is the most common form of MODY, accounting for more than half the cases of MODY. Patients with this condition and with MODY1 caused by mutations in HNF1A and MODY12 caused by mutations in ABCC8 are extremely sensitive to sulfonylureas, which are considered first-line therapy in these patients [117–119]. Patients with HNF1A MODY had a 5.2-fold greater reduction in fasting plasma glucose with gliclazide than with metformin and 3.9-fold greater response to gliclazide than those patients with T2D [120].
Mechanistic links between vitamin deficiencies and diabetes mellitus: a review
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Tajudeen O. Yahaya, AbdulRahman B. Yusuf, Jamilu K. Danjuma, Bello M. Usman, Yahaya M. Ishiaku
The term diabetes mellitus (DM) describes several distinct metabolic disorders characterized by high blood glucose (hyperglycemia) [1]. Diabetes mellitus was previously tagged a disease associated with ‘sweet urine’ and high muscle loss [2]. The initial notion stemmed from the sweet taste of the urine of diabetics due to the leakage of glucose accumulated in the blood into the urine. Type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM) are the two most common subtypes of DM[1]. Most often, T1DM begins when the immune system dysfunctionally destroys the pancreatic β-cells that produce insulin and causes an accumulation of glucose in the blood [3]. The main features of T2DM are insufficient insulin, or insulin resistance – a condition in which the body cells fail to utilize insulin [4]. Other forms of DM include gestational diabetes mellitus, maturity-onset diabetes of the young (MODY), and neonatal diabetes mellitus [3,5,6]. Major symptoms of DM include thirst, polyuria, blurred vision, emaciation, and genital yeast infections [1].