Lifestyle Therapies for the Management of Diabetes
James M. Rippe in Lifestyle Medicine, 2019
Type 1 diabetes accounts for approximately 5% of diagnosed diabetes and is due to cellular-mediated autoimmune destruction of the pancreatic beta-cells, usually leading to absolute insulin deficiency.1 The rate of beta-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Immune-mediated diabetes commonly occurs in childhood and adolescence, but it can occur at any age, even in the eighth and ninth decades of life.8 Children and adolescents may present with ketoacidosis as the first symptom of the disease. Adults may retain sufficient beta-cell function to prevent ketoacidosis for many years; however, such individuals eventually become dependent on insulin for survival and are at risk for ketoacidosis. This later-onset type 1 diabetes picture is referred to as Latent Autoimmune Diabetes of Adults (LADA).
Diabetes in Older Adults and Its Management
K. Rao Poduri in Geriatric Rehabilitation, 2017
Type 2 diabetes refers to the remainder of patients with diabetes. There is a strong familial predisposition, so that if one of two identical twins develops type 2 diabetes, the second has a >90% chance of developing the disease. These patients develop diabetes because their beta cells cannot produce sufficient insulin to meet their requirements for glycemic/metabolic regulation (3). People with type 2 diabetes are usually resistant to insulin and, as a group, are obese. These people constitute more than 90% of older patients with diabetes in whom diabetes prevalence increases with age. Unless specifically indicated, most of the remainder of this chapter deals with type 2 diabetes. An interesting form of diabetes, which has been described in the past 23 years, is Latent Autoimmune Diabetes in Adults (LADA). These patients were originally described among a population of people with type 2 diabetes. Such patients were leaner, had glutamic acid decarboxylase or islet cell antibodies, higher HbA1C, and >90% required insulin within 6 years versus 16% of type 2 patients who were antibody-negative (6). Disagreement exists as to whether these LADA patients have type 1, type 2, or their own peculiar form of diabetes. Moreover, the natural history of diagnosed type 2 diabetes is progressive beta cell dysfunction, often requiring insulin treatment (6,7).
Carbohydrate metabolism
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
Previously called insulin-dependent diabetes mellitus, this is the term used to describe the condition in patients for whom insulin therapy is essential because they are prone to develop ketoacidosis. It usually presents during childhood or adolescence. Most of these cases are due to immune-mediated processes and may be associated with other autoimmune disorders such as Addison’s disease, vitiligo and Hashimoto’s thyroiditis. It has been suggested that many cases follow a viral infection that has damaged the β-cells of the pancreatic islets. Individuals most at risk are those with human leucocyte antigen (HLA) types DR3 and DR4 of the major histocompatibility complex. Autoantibodies to islet cells, insulin, tyrosine phosphatases IA-2 and IA-2β and glutamic decarboxylase (GAD) are found in about 90 per cent of cases. There is a form of type 1 diabetes called idiopathic diabetes mellitus that is not autoimmune mediated but is strongly inherited and more common in black and Asian people. The insulin requirement of affected people can fluctuate widely and the cause is unknown. There is also LADA (latent autoimmune diabetes of adults), sometimes called slow-onset type 1 diabetes.
Prediction, diagnosis, prevention and treatment: genetic-led care of patients with diabetes
Published in Expert Review of Precision Medicine and Drug Development, 2021
Watip Tangjittipokin, Nutsakol Borrisut, Patcharapong Rujirawan
Latent autoimmune diabetes of adults (LADA) is one of autoimmune diabetes spectrum that shared clinical manifestation and metabolic profile from both T1DM and T2DM. Although, patients with LADA have common characteristics that provide the clue for diagnoses such as age <50, family or personal history of autoimmunity, low BMI, or acute symptom onset; however; current key for LADA diagnosis still need the presence of diabetes-associated autoantibodies (90% of subjects autoantibodies are GADA positive [8]) along with adult-onset (age > 30) and absence of insulin requirement for at least 6 months after diagnosis [9]. LADA patients tend to have a similar or higher frequency of metabolic syndromes than adult-onset T1DM but have lower metabolic syndromes such as lower insulin resistance, blood pressure, and diabetic dyslipidemia than T2DM [10]. LADA patients also have lower major cardiovascular risk both clinical and metabolic parameters after adjustment for traditional cardiovascular risk factors and lower risk of microvascular complication compare to T2DM patients [11,12].
Auto-reactivity against gut bacterial peptides in patients with late-onset diabetes
Published in Autoimmunity, 2020
Mohammad Sajid, Krishna Biswas, Harpreet Singh, Sapna Negi
Diabetes mellitus is a non-communicable disease causing a burden for global human health. In 2017, worldwide there were approximately 451 million individuals who had diabetes mellitus (DM) and with the current trend, it is expected to reach 693 million by 2045 [1]. Approximately 90–95% of DM belongs to type 2 diabetes (T2D). It is essential to predict DM and prevent it in time, for which we need to understand the disease completely. The main triggers of this disease are an unhealthy lifestyle, obesity, and advanced age. The mounting inflammatory response in T2D is assigned through autoimmunity [2]. Further, another adult-onset autoimmune diabetic condition is known as Latent autoimmune diabetes in adults (LADA) and this phenotype mainly does not need insulin therapy [3]. Most of the T2D is mainly due to insulin resistance [4]. T2D is known to be a metabolic disorder. In this study, we hypothesize that sera binding of some metabolic peptides might cause a spectrum of diseases including T2D.
The association between rs1893217, rs478582 in PTPN2 and T1D risk with different diagnosed age, and related clinical characteristics in Chinese Han population
Published in Autoimmunity, 2019
Shu Chen, Hongqi Fan, Yingjie Feng, Yuyue Zhang, Yang Chen, Yong Gu, Yun Shi, Hao Dai, Mei Zhang, Xinyu Xu, Heng Chen, Tao Yang, Kuanfeng Xu
A total of 1023 unrelated T1D patients and 1247 healthy controls were recruited from the First Affiliated Hospital of Nanjing Medical University between January 2008 and December 2016. T1D was diagnosed according to the World Health Organization (WHO) criteria and with at least one autoantibody positive (ZnT8A, GADA, IA-2A or IAA). In addition, we further excluded patients that had clinical features of latent autoimmune diabetes in adults (LADA). Clinical characteristics of all subjects are listed in Table S1. Healthy controls were enrolled from the same geographical region without diabetes or overt autoimmune diseases. Informed consent was obtained from all the subjects included or their guardians in a written way, and study population was determined as Chinese Han by questionnaire. The study was approved by the Ethics Committee from the First Affiliated Hospital of Nanjing Medical University.
Related Knowledge Centers
- Diabetes
- Differential Diagnosis
- Glutamate Decarboxylase
- Type 1 Diabetes
- Type 2 Diabetes
- Insulin Resistance
- Polydipsia
- Polyuria
- C-Peptide
- Diabetic Ketoacidosis