scholarly journals Effects of an inhibitor of 3beta-hydroxysteroid dehydrogenase on glucose, lipid metabolism and adipose tissue in a patient with type 2 diabetes, complicated with Cushing’s syndrome

Author(s):  
Yanai
Author(s):  
Ziadoon Faisal ◽  
Miguel Debono

Summary In this case report, we describe the management of a patient who was admitted with an ectopic ACTH syndrome during the COVID pandemic with new-onset type 2 diabetes, neutrophilia and unexplained hypokalaemia. These three findings when combined should alert physicians to the potential presence of Cushing’s syndrome (CS). On admission, a quick diagnosis of CS was made based on clinical and biochemical features and the patient was treated urgently using high dose oral metyrapone thus allowing delays in surgery and rapidly improving the patient’s clinical condition. This resulted in the treatment of hyperglycaemia, hypokalaemia and hypertension reducing cardiovascular risk and likely risk for infection. Observing COVID-19 pandemic international guidelines to treat patients with CS has shown to be effective and offers endocrinologists an option to manage these patients adequately in difficult times. Learning points This case report highlights the importance of having a low threshold for suspicion and investigation for Cushing’s syndrome in a patient with neutrophilia and hypokalaemia, recently diagnosed with type 2 diabetes especially in someone with catabolic features of the disease irrespective of losing weight. It also supports the use of alternative methods of approaching the diagnosis and treatment of Cushing’s syndrome during a pandemic as indicated by international protocols designed specifically for managing this condition during Covid-19.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nicholas J. Carruthers ◽  
Clarissa Strieder-Barboza ◽  
Joseph A. Caruso ◽  
Carmen G. Flesher ◽  
Nicki A. Baker ◽  
...  

AbstractDysfunctional visceral adipose tissue (VAT) in obesity is associated with type 2 diabetes (DM) but underlying mechanisms remain unclear. Our objective in this discovery analysis was to identify genes and proteins regulated by DM to elucidate aberrant cellular metabolic and signaling mediators. We performed label-free proteomics and RNA-sequencing analysis of VAT from female bariatric surgery subjects with DM and without DM (NDM). We quantified 1965 protein groups, 23 proteins, and 372 genes that were differently abundant in DM vs. NDM VAT. Proteins downregulated in DM were related to fatty acid synthesis and mitochondrial function (fatty acid synthase, FASN; dihydrolipoyl dehydrogenase, mitochondrial, E3 component, DLD; succinate dehydrogenase-α, SDHA) while proteins upregulated in DM were associated with innate immunity and transcriptional regulation (vitronectin, VTN; endothelial protein C receptor, EPCR; signal transducer and activator of transcription 5B, STAT5B). Transcriptome indicated defects in innate inflammation, lipid metabolism, and extracellular matrix (ECM) function, and components of complement classical and alternative cascades. The VAT proteome and transcriptome shared 13 biological processes impacted by DM, related to complement activation, cell proliferation and migration, ECM organization, lipid metabolism, and gluconeogenesis. Our data revealed a marked effect of DM in downregulating FASN. We also demonstrate enrichment of complement factor B (CFB), coagulation factor XIII A chain (F13A1), thrombospondin 1 (THBS1), and integrins at mRNA and protein levels, albeit with lower q-values and lack of Western blot or PCR confirmation. Our findings suggest putative mechanisms of VAT dysfunction in DM.


2012 ◽  
Vol 97 (10) ◽  
pp. 3467-3475 ◽  
Author(s):  
Massimo Terzolo ◽  
Giuseppe Reimondo ◽  
Iacopo Chiodini ◽  
Roberto Castello ◽  
Roberta Giordano ◽  
...  

Endocrine ◽  
2018 ◽  
Vol 62 (1) ◽  
pp. 116-128 ◽  
Author(s):  
Cherno O. Sidibeh ◽  
Maria J. Pereira ◽  
Xesus M. Abalo ◽  
Gretha J. Boersma ◽  
Stanko Skrtic ◽  
...  

2011 ◽  
Vol 31 (6) ◽  
pp. 541-541 ◽  
Author(s):  
R. Schiemer ◽  
M. Latibeaudiere ◽  
C. Close ◽  
R. Fox

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