Ketosis-onset diabetes without islet-associated autoantibodies in a patient with MELAS.

Takamura, Toshiji; Nagai, Yukihiro; Torita, Muneyoshi; Yamashita, Hitoshi; Kahara, Toshio; Koshino, Yoshitaka; Kobayashi, Kazuma

doi:10.2337/diacare.23.7.1018

Cited by 4 publications

(2 citation statements)

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“…Although ketosis onset diabetes is sometimes called KPD, both present with DKA or unprovoked ketosis, KPD is defined as a widespread, emerging, heterogeneous syndrome which does not necessarily have the typical phenotype of autoimmune T1DM [18, 19], but ketosis onset diabetic patients present with ketosis or ketoacidosis without known diabetes [20, 21]. So we select this group to study.…”

Section: Discussionmentioning

confidence: 99%

Ketosis Onset Type 2 Diabetes Had Better Isletβ-Cell Function and More Serious Insulin Resistance

Zeng

et al. 2014

Journal of Diabetes Research

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Diabetic ketosis had been identified as a characteristic of type 1 diabetes mellitus (T1DM), but now emerging evidence has identified that they were diagnosed as T2DM after long time follow up. This case control study was aimed at comparing the clinical characteristic, β-cell function, and insulin resistance of ketosis and nonketotic onset T2DM and providing evidence for treatment selection. 140 cases of newly diagnosed T2DM patients were divided into ketosis (62 cases) and nonketotic onset group (78 cases). After correction of hyperglycemia and ketosis with insulin therapy, plasma C-peptide concentrations were measured at 0, 0.5, 1, 2, and 3 hours after 75 g glucose oral administration. Area under the curve (AUC) of C-peptide was calculated. Homoeostasis model assessment was used to estimate basal β-cell function (HOMA-β) and insulin resistance (HOMA-IR). Our results showed that ketosis onset group had higher prevalence of nonalcoholic fatty liver disease (NAFLD) than nonketotic group (P = 0.04). Ketosis onset group had increased plasma C-peptide levels at 0 h, 0.5 h, and 3 h and higher AUC0–0.5, AUC0–1, AUC0–3 (P < 0.05). Moreover, this group also had higher HOMA-β and HOMA-IR than nonketotic group (P < 0.05). From these data, we concluded that ketosis onset T2DM had better islet β-cell function and more serious insulin resistance than nonketotic onset T2DM.

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Section: Discussionmentioning

confidence: 99%

Ketosis Onset Type 2 Diabetes Had Better Isletβ-Cell Function and More Serious Insulin Resistance

Zeng

et al. 2014

Journal of Diabetes Research

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“…Ketosis-prone diabetes (KPD) is defined as a widespread, emerging, heterogeneous syndrome characterized by patients who present with DKA or unprovoked ketosis but do not necessarily have the typical phenotype of autoimmune type 1 diabetes [7, 8]. While ketosis-onset diabetes patients present with ketosis or ketoacidosis without known diabetes [9, 10], some investigators defined ketosis-onset diabetes as diabetes with the presence of diabetic ketosis and in the absence of glutamic acid decarboxylase (GAD) and tyrosin phosphatase (IA-2) autoantibodies. We choose patients separately fit for each of the above conditions to study.…”

Section: Introductionmentioning

confidence: 99%

Ketosis-Onset Diabetes and Ketosis-Prone Diabetes: Same or Not?

Liu

et al. 2013

International Journal of Endocrinology

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Objective. To compare clinical characteristics, immunological markers, and β-cell functions of 4 subgroups (“Aβ” classification system) of ketosis-onset diabetes and ketosis prone diabetes patients without known diabetes, presenting with ketosis or diabetic ketoacidosis (DKA) and admitted to our department from March 2011 to December 2011 in China, with 50 healthy persons as control group. Results. β-cell functional reserve was preserved in 63.52% of patients. In almost each subgroup (except A− β− subgroup of ketosis prone group), male patients were more than female ones. The age of the majority of patients in ketosis prone group was older than that of ketosis-onset group, except A− β− subgroup of ketosis prone group. The durations from the patient first time ketosis or DKA onset to admitting to the hospital have significant difference, which were much longer for the ketosis prone group except the A+ β+ subgroup. BMI has no significant difference among subgroups. FPG of ketosis prone group was lower than that of A− β+ subgroup and A+ β+ subgroup in ketosis-onset group. A− β− subgroup and A+ β+ subgroup of ketosis prone group have lower HbA1c than ketosis-onset group. Conclusions. Ketosis-onset diabetes and ketosis prone diabetes do not absolutely have the same clinical characteristics. Each subgroup shows different specialty.

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Not quite type 1 or type 2, what now? Review of monogenic, mitochondrial, and syndromic diabetes

Yeung

Hannah‐Shmouni

Niederhoffer

et al. 2018

Rev Endocr Metab Disord

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Diabetes mellitus is a heterogeneous group of conditions defined by resultant chronic hyperglycemia. Given the increasing prevalence of diabetes mellitus and the increasing understanding of genetic etiologies, we present a broad review of rare genetic forms of diabetes that have differing diagnostic and/or treatment implications from type 1 and type 2 diabetes. Advances in understanding the genotype-phenotype associations in these rare forms of diabetes offer clinically available examples of evolving precision medicine where defining the correct genetic etiology can radically alter treatment approaches. In this review, we focus on forms of monogenic diabetes, mitochondrial diabetes, and syndromic diabetes.

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Ketosis-onset diabetes without islet-associated autoantibodies in a patient with MELAS.

Cited by 4 publications

References 0 publications

Ketosis Onset Type 2 Diabetes Had Better Isletβ-Cell Function and More Serious Insulin Resistance

Ketosis Onset Type 2 Diabetes Had Better Isletβ-Cell Function and More Serious Insulin Resistance

Ketosis-Onset Diabetes and Ketosis-Prone Diabetes: Same or Not?

Not quite type 1 or type 2, what now? Review of monogenic, mitochondrial, and syndromic diabetes

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