scholarly journals Studies on the pathogenesis of lipoatrophic diabetes: A case of congenital systemic absence of adipose tissue associated with insulin-resistant diabetes mellitus and hepatosplenomegaly

Diabetologia ◽  
1972 ◽  
Vol 8 (5) ◽  
pp. 319-325 ◽  
Author(s):  
J. Taton ◽  
B. Malczewski ◽  
A. Wisniewska
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Insulin Resistant ◽  
Lipoatrophic Diabetes

scholarly journals Combination of lipoatrophic diabetes mellitus with systemic scleroderma and phenylketonuria

2017 ◽  
Vol 63 (2) ◽  
pp. 130-133
Author(s):  
Galina N. Svetlova ◽  
Tamara L. Kuraeva ◽  
Dmitriy L. Alekseev ◽  
Valentina A. Peterkova
Keyword(s):  
Diabetes Mellitus ◽  
Molecular Genetic ◽  
Clinical Manifestations ◽  
Molecular Genetic Analysis ◽  
Systemic Scleroderma ◽  
Dietary Regimen ◽  
Insulin Resistant ◽  
Lipoatrophic Diabetes ◽  
Liver Functions ◽  
High Doses

We present the first report of a rare form of lipoatrophic diabetes mellitus in a child with partial autoimmune lipodystrophy combined with systemic scleroderma and phenylketonuria. We describe the features of clinical manifestations, diagnosis, and therapy. To exclude the monogenic form of lipodystrophy, we performed a molecular genetic analysis of genes ZMPSTE24, LMNA, BSCL2, PLIN1, PTRF, LMNB2, POLD1, AKT2, CIDEC, PIK3CA, PPARG, PSMB8, CAV1, PPP1R3A, and AGPAT2 that are responsible for the development of lipodystrophy and insulin resistance. No mutations were found. The presence of systemic scleroderma of autoimmune genesis enabled the diagnosis of autoimmune lipodystrophy. Treatment of insulin-resistant diabetes mellitus in lipodystrophy is a challenge: biguanide therapy is dangerous due to impairment of liver functions, and insulin therapy is not effective enough; administration of high doses is required. The presence of phenylketonuria further complicates compliance with the dietary regimen. The combination of three rare diseases ― lipoatrophic diabetes, phenylketonuria, and systemic scleroderma ― in one patient has not been found in the available literature.

Diabetes, lipids, and adipocyte secretagogues

2004 ◽  
Vol 82 (1) ◽  
pp. 170-190 ◽  
Author(s):  
May Faraj ◽  
Hui Ling Lu ◽  
Katherine Cianflone
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
White Adipose Tissue ◽  
Insulin Response ◽  
Type Ii Diabetes Mellitus ◽  
Insulin Resistant ◽  
Glucose And Lipid Metabolism ◽  
Obesity And Diabetes ◽  
Factor Α

That obesity is associated with insulin resistance and type II diabetes mellitus is well accepted. Overloading of white adipose tissue beyond its storage capacity leads to lipid disorders in non-adipose tissues, namely skeletal and cardiac muscles, pancreas, and liver, effects that are often mediated through increased non-esterified fatty acid fluxes. This in turn leads to a tissue-specific disordered insulin response and increased lipid deposition and lipotoxicity, coupled to abnormal plasma metabolic and (or) lipoprotein profiles. Thus, the importance of functional adipocytes is crucial, as highlighted by the disorders seen in both "too much" (obesity) and "too little" (lipodystrophy) white adipose tissue. However, beyond its capacity for fat storage, white adipose tissue is now well recognised as an endocrine tissue producing multiple hormones whose plasma levels are altered in obese, insulin-resistant, and diabetic subjects. The consequence of these hormonal alterations with respect to both glucose and lipid metabolism in insulin target tissues is just beginning to be understood. The present review will focus on a number of these hormones: acylation-stimulating protein, leptin, adiponectin, tumour necrosis factor α, interleukin-6, and resistin, defining their changes induced in obesity and diabetes mellitus and highlighting their functional properties that may protect or worsen lipid metabolism.Key words: C3adesarg, fatty acid trapping, lipolysis, lipogenesis.

Evidence of insulin resistant lipid metabolism in adipose tissue in familial combined hyperlipidemia, but not type 2 diabetes mellitus

2002 ◽  
Vol 164 (2) ◽  
pp. 337-346 ◽  
Author(s):  
Carla J.H van der Kallen ◽  
Christine Voors-Pette ◽  
Freek G Bouwman ◽  
Hans A Keizer ◽  
Jinyan Y Lu ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Familial Combined Hyperlipidemia ◽  
Insulin Resistant

Expression of adiponectin gene and adiponectin receptors in placental and adipose tissue in women with gestational diabetes mellitus

2013 ◽  
Author(s):  
Beata Matyjaszek-Matuszek ◽  
Mariusz Kowalczyk ◽  
Agnieszka Lagowska-Batyra ◽  
Wojciech Gernand ◽  
Andrzej Nowakowski ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Adiponectin Gene ◽  
Adiponectin Receptors

Does intra-abdominal adipose tissue in black men determine whether NIDDM is insulin-resistant or insulin-sensitive?

Diabetes ◽  
1995 ◽  
Vol 44 (2) ◽  
pp. 141-146 ◽  
Author(s):  
M. A. Banerji ◽  
R. L. Chaiken ◽  
D. Gordon ◽  
J. G. Kral ◽  
H. E. Lebovitz
Keyword(s):  
Adipose Tissue ◽  
Black Men ◽  
Abdominal Adipose Tissue ◽  
Insulin Resistant

Insulin Therapy in Pregnancy Hypertensive Diseases and its Effect on the Offspring and Mother Later in Life

2019 ◽  
Vol 17 (5) ◽  
pp. 455-464 ◽  
Author(s):  
Alfonso Mate ◽  
Antonio J. Blanca ◽  
Rocío Salsoso ◽  
Fernando Toledo ◽  
Pablo Stiefel ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Polycystic Ovary Syndrome ◽  
Insulin Therapy ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Insulin Resistant ◽  
Hypertensive Disorders ◽  
The Impact ◽  
In Pregnancy

Pregnancy hypertensive disorders such as Preeclampsia (PE) are strongly correlated with insulin resistance, a condition in which the metabolic handling of D-glucose is deficient. In addition, the impact of preeclampsia is enhanced by other insulin-resistant disorders, including polycystic ovary syndrome and obesity. For this reason, there is a clear association between maternal insulin resistance, polycystic ovary syndrome, obesity and the development of PE. However, whether PE is a consequence or the cause of these disorders is still unclear. Insulin therapy is usually recommended to pregnant women with diabetes mellitus when dietary and lifestyle measures have failed. The advantage of insulin therapy for Gestational Diabetes Mellitus (GDM) patients with hypertension is still controversial; surprisingly, there are no studies in which insulin therapy has been used in patients with hypertension in pregnancy without or with an established GDM. This review is focused on the use of insulin therapy in hypertensive disorders in the pregnancy and its effect on offspring and mother later in life. PubMed and relevant medical databases have been screened for literature covering research in the field especially in the last 5-10 years.

scholarly journals Gestational Diabetes Mellitus and Infant Adiposity at Birth: A Systematic Review and Meta-Analysis of Therapeutic Interventions

2021 ◽  
Vol 10 (4) ◽  
pp. 835
Author(s):  
Manoja P. Herath ◽  
Jeffrey M. Beckett ◽  
Andrew P. Hills ◽  
Nuala M. Byrne ◽  
Kiran D. K. Ahuja
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Later Life ◽  
Therapeutic Interventions ◽  
Increased Risk ◽  
The Impact

Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.

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