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Article ; Online: Editorial for "MR Assessed Changes of Renal Sinus Fat in Response to Glucose Regulation in West European and South Asian Patients With Type 2 Diabetes".

Kuchay, Mohammad Shafi / Martínez-Montoro, José Ignacio

Journal of magnetic resonance imaging : JMRI

2023

Language	English
Publishing date	2023-12-13
Publishing country	United States
Document type	Editorial
ZDB-ID	1146614-5
ISSN	1522-2586 ; 1053-1807
ISSN (online)	1522-2586
ISSN	1053-1807
DOI	10.1002/jmri.29175
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Zs.A 3648: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 236: Show issues

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Article ; Online: Sodium-glucose cotransporter-2 inhibitors as first-line pharmacological therapy for type 2 diabetes?

Kuchay, Mohammad Shafi / Misra, Anoop

Diabetes & metabolic syndrome

2022 Volume 16, Issue 8, Page(s) 102580

MeSH term(s)	Canagliflozin ; Diabetes Mellitus, Type 2 ; Glucose ; Humans ; Hypoglycemic Agents ; Sodium ; Sodium-Glucose Transporter 2 Inhibitors
Chemical Substances	Hypoglycemic Agents ; Sodium-Glucose Transporter 2 Inhibitors ; Canagliflozin (0SAC974Z85) ; Sodium (9NEZ333N27) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-07-21
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2022.102580
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Article ; Online: Toll-like receptors and metabolic (dysfunction)-associated fatty liver disease.

Khanmohammadi, Shaghayegh / Kuchay, Mohammad Shafi

Pharmacological research

2022 Volume 185, Page(s) 106507

Abstract: Metabolic (dysfunction)-associated fatty liver disease (MAFLD) is characterized by the accumulation of lipids in the liver (steatosis). In predisposed individuals, liver steatosis can progress to inflammation, fibrosis, cirrhosis, and hepatocellular ... ...

Abstract	Metabolic (dysfunction)-associated fatty liver disease (MAFLD) is characterized by the accumulation of lipids in the liver (steatosis). In predisposed individuals, liver steatosis can progress to inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of MAFLD is complex and incompletely understood, involving various steatogenic, pro-inflammatory, and fibrogenic processes. Hyperactivation of the innate immune system through hepatic toll-like receptors (TLRs) contributes to the pathogenesis of MAFLD. Products of intestinal microbiota and danger signals from damaged hepatocytes constitute key ligands of TLRs that promote MAFLD. Most TLRs promote development and progression of MAFLD by induction of pro-inflammatory and pro-fibrogenic cytokines. Several nutraceutical and therapeutic agents improve MAFLD partly through the inhibition of hepatic TLRs. Herein, we review the available literature on hepatic TLR expression and signaling; crosstalk between gut microbiota and hepatic TLRs; and the contribution of TLRs to the pathogenesis of MAFLD. We also highlight implications for therapeutic approaches for MAFLD based on modulation of TLR signaling.
MeSH term(s)	Humans ; Toll-Like Receptors/metabolism ; Fatty Liver ; Liver Cirrhosis/metabolism ; Liver Neoplasms ; Non-alcoholic Fatty Liver Disease/metabolism
Chemical Substances	Toll-Like Receptors
Language	English
Publishing date	2022-10-14
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2022.106507
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 721: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Role of diabetologists in the management of nonalcoholic fatty liver disease: Primary prevention and screening/management of fibrosis and cirrhosis.

Kuchay, Mohammad Shafi / Misra, Anoop

Diabetes & metabolic syndrome

2022 Volume 16, Issue 3, Page(s) 102446

Abstract: Background and aims: Nonalcoholic fatty liver disease (NAFLD) is a common condition, especially among individuals with type 2 diabetes (T2D). Presence of T2D increases the risk of progression of simple steatosis to more severe liver conditions, such as ... ...

Abstract	Background and aims: Nonalcoholic fatty liver disease (NAFLD) is a common condition, especially among individuals with type 2 diabetes (T2D). Presence of T2D increases the risk of progression of simple steatosis to more severe liver conditions, such as nonalcoholic steatohepatitis (NASH) and fibrosis (NASH-fibrosis). Since majority of patients with T2D are managed by diabetologists (including physicians and endocrinologists), their roles in the management of coexisting NAFLD are not well defined, partly due to lack of unambiguous guidelines. Methods: A literature search was performed with Medline (PubMed), Scopus and Google Scholar electronic databases till January 2022, using relevant keywords (nonalcoholic fatty liver disease and diabetologist; screening of NASH; management of NASH) to extract relevant studies describing prevention and screening of NAFLD/NASH, especially in people with T2D. Results: Diabetologists have two main roles for the management of patients with T2D and coexisting NAFLD. The most important role is to prevent the development of NASH-fibrosis in patients with simple steatosis (primary prevention). This can be achieved by reinforcing the importance of lifestyle measures, and by early use of glucose-lowering agents with beneficial effects on the liver. The second important role of diabetologists is to screen all patients with T2D for liver fibrosis and compensated cirrhosis, and provide appropriate referral for timely management of complications (secondary prevention). Conclusion: Diabetologists can play a central role in mitigating the epidemic of NAFLD in individuals with T2D. However, diabetologists need to be aware about their roles in NASH-fibrosis prevention and screening. Furthermore, longitudinal studies should explore the role of newer glucose-lowering drugs in the primary prevention of NASH-fibrosis in individuals with coexisting T2D and simple steatosis.
MeSH term(s)	Diabetes Mellitus, Type 2/complications ; Humans ; Liver ; Liver Cirrhosis/diagnosis ; Liver Cirrhosis/etiology ; Liver Cirrhosis/prevention & control ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/prevention & control ; Physicians ; Primary Prevention
Language	English
Publishing date	2022-02-28
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2022.102446
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: NOD-like receptors in the pathogenesis of metabolic (dysfunction)-associated fatty liver disease: Therapeutic agents targeting NOD-like receptors.

Khanmohammadi, Shaghayegh / Ramos-Molina, Bruno / Kuchay, Mohammad Shafi

Diabetes & metabolic syndrome

2023 Volume 17, Issue 7, Page(s) 102788

Abstract: Background and aims: In metabolic (dysfunction)-associated fatty liver disease (MAFLD), activation of inflammatory processes marks the transition of simple steatosis to steatohepatitis, which can further evolve to advanced fibrosis or hepatocellular ... ...

Abstract	Background and aims: In metabolic (dysfunction)-associated fatty liver disease (MAFLD), activation of inflammatory processes marks the transition of simple steatosis to steatohepatitis, which can further evolve to advanced fibrosis or hepatocellular carcinoma. Under the stress of chronic overnutrition, the innate immune system orchestrates hepatic inflammation through pattern recognition receptors (PRRs). Cytosolic PRRs that include NOD-like receptors (NLRs) are crucial for inducing inflammatory processes in the liver. Methods: A literature search was performed with Medline (PubMed), Google Scholar and Scopus electronic databases till January 2023, using relevant keywords to extract studies describing the role of NLRs in the pathogenesis of MAFLD. Results: Several NLRs operate through the formation of inflammasomes, which are multimolecular complexes that generate pro-inflammatory cytokines and induce pyroptotic cell death. A multitude of pharmacological agents target NLRs and improve several aspects of MAFLD. In this review, we discuss the current concepts related to the role of NLRs in the pathogenesis of MAFLD and its complications. We also discuss the latest research on MAFLD therapeutics functioning through NLRs. Conclusions: NLRs play a significant role in the pathogenesis of MAFLD and its consequences, especially through generation of inflammasomes, such as NLRP3 inflammasomes. Lifestyle changes (exercise, coffee consumption) and therapeutic agents (GLP-1 receptor agonists, sodium-glucose cotransporter-2 inhibitors, obeticholic acid) improve MAFLD and its complications partly through blockade of NLRP3 inflammasome activation. New studies are required to explore these inflammatory pathways fully for the treatment of MAFLD.
MeSH term(s)	Humans ; Inflammasomes/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLR Proteins ; Non-alcoholic Fatty Liver Disease ; Receptors, Pattern Recognition ; Sodium-Glucose Transporter 2 Inhibitors
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLR Proteins ; Receptors, Pattern Recognition ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2023-06-04
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2023.102788
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: From non-alcoholic fatty liver disease (NAFLD) to metabolic-associated fatty liver disease (MAFLD): A journey over 40 years.

Kuchay, Mohammad Shafi / Misra, Anoop

Diabetes & metabolic syndrome

2020 Volume 14, Issue 4, Page(s) 695–696

MeSH term(s)	Fatty Liver/etiology ; Fatty Liver/pathology ; Humans ; Metabolic Syndrome/complications ; Non-alcoholic Fatty Liver Disease/physiopathology ; Terminology as Topic
Language	English
Publishing date	2020-05-13
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2020.05.019
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Article ; Online: Empagliflozin induced euglycemic diabetic ketoacidosis in a patient undergoing coronary artery bypass graft despite discontinuation of the drug 48 hours prior to the surgery.

Kuchay, Mohammad Shafi / Mishra, Sunil Kumar / Mehta, Yatin

Diabetes & metabolic syndrome

2021 Volume 15, Issue 3, Page(s) 909–911

MeSH term(s)	Benzhydryl Compounds/adverse effects ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/surgery ; Coronary Artery Bypass/adverse effects ; Diabetes Mellitus, Type 2/complications ; Diabetic Ketoacidosis/etiology ; Diabetic Ketoacidosis/pathology ; Female ; Glucosides/adverse effects ; Humans ; Middle Aged ; Prognosis ; Sodium-Glucose Transporter 2 Inhibitors/adverse effects
Chemical Substances	Benzhydryl Compounds ; Glucosides ; Sodium-Glucose Transporter 2 Inhibitors ; empagliflozin (HDC1R2M35U)
Language	English
Publishing date	2021-04-22
Publishing country	Netherlands
Document type	Case Reports
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2021.04.016
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Article: Liver cirrhosis and sarcopenia: a dreadful combination.

Kuchay, Mohammad Shafi / Martínez-Montoro, José Ignacio / Llamoza-Torres, Camilo Julio / Fernández-García, José Carlos / Ramos-Molina, Bruno

Hepatobiliary surgery and nutrition

2022 Volume 11, Issue 5, Page(s) 729–731

Language	English
Publishing date	2022-10-21
Publishing country	China (Republic : 1949- )
Document type	Editorial ; Comment
ZDB-ID	2812398-0
ISSN	2304-389X ; 2304-3881
ISSN (online)	2304-389X
ISSN	2304-3881
DOI	10.21037/hbsn-22-355
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Pathophysiological mechanisms underlying MAFLD.

Kuchay, Mohammad Shafi / Choudhary, Narendra Singh / Mishra, Sunil Kumar

Diabetes & metabolic syndrome

2020 Volume 14, Issue 6, Page(s) 1875–1887

Abstract: Background and aims: The pathophysiology underlying metabolic associated fatty liver disease (MAFLD) involves a multitude of interlinked processes, including insulin resistance (IR) underlying the metabolic syndrome, lipotoxicity attributable to the ... ...

Abstract	Background and aims: The pathophysiology underlying metabolic associated fatty liver disease (MAFLD) involves a multitude of interlinked processes, including insulin resistance (IR) underlying the metabolic syndrome, lipotoxicity attributable to the accumulation of toxic lipid species, infiltration of proinflammatory cells causing hepatic injury and ultimately leading to hepatic stellate cell (HSC) activation and fibrogenesis. The proximal processes, such as IR, lipid overload and lipotoxicity are relatively well established, but the downstream molecular mechanisms, such as inflammatory processes, hepatocyte lipoapoptosis, and fibrogenesis are incompletely understood. Methods: A literature search was performed with Medline (PubMed), Scopus and Google Scholar electronic databases till June 2020, using relevant keywords (nonalcoholic fatty liver disease; metabolic associated fatty liver disease; nonalcoholic steatohepatitis; NASH pathogenesis) to extract relevant studies describing pathogenesis of MAFLD/MASH. Results: Several studies have reported new concepts underlying pathophysiology of MAFLD. Activation of HSCs is the common final pathway for diverse signals from damaged hepatocytes and proinflammatory cells. Activated HSCs then secrete excess extracellular matrix (ECM) which accumulates and impairs structure and function of the liver. TAZ (a transcriptional regulator), hedgehog (HH) ligands, transforming growth factor-β (TGF-β), bone morphogenetic protein 8B (BMP8B) and osteopontin play important roles in activating these HSCs. Dysfunctional gut microbiome, dysregulated bile acid metabolism, endogenous alcohol production, and intestinal fructose handling, modify individual susceptibility to MASH. Conclusions: Newer concepts of pathophysiology underlying MASH, such as TAZ/Ihh pathway, extracellular vesicles, microRNA, dysfunctional gut microbiome and intestinal fructose handling present promising targets for the development of therapeutic agents.
MeSH term(s)	Animals ; Gene Expression Regulation ; Humans ; Non-alcoholic Fatty Liver Disease/physiopathology ; Signal Transduction
Language	English
Publishing date	2020-09-24
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2273766-2
ISSN	1878-0334 ; 1871-4021
ISSN (online)	1878-0334
ISSN	1871-4021
DOI	10.1016/j.dsx.2020.09.026
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Denosumab can be used successfully as a bridge to surgery in patients with severe hypercalcemia due to primary hyperparathyroidism.

Kuchay, Mohammad Shafi / Mathew, Anu / Kaur, Parjeet / Mishra, Sunil Kumar

Archives of endocrinology and metabolism

2021 Volume 65, Issue 5, Page(s) 669–673

Abstract: Severe hypercalcemia is a medical emergency that requires immediate and aggressive management. Primary hyperparathyroidism (PHPT) often causes severe hypercalcemia. Volume resuscitation, parenteral salmon calcitonin, and administration of intravenous ... ...

Abstract	Severe hypercalcemia is a medical emergency that requires immediate and aggressive management. Primary hyperparathyroidism (PHPT) often causes severe hypercalcemia. Volume resuscitation, parenteral salmon calcitonin, and administration of intravenous bisphosphonates are common measures used to stabilize patients. However, the use of these measures is inadequate in several patients and may even be contraindicated in individuals with renal insufficiency or severe systemic illness. This study demonstrated the efficacy and safety of denosumab in patients with severe hypercalcemia due to PHPT, when immediate surgery was not feasible. We present four patients with severe hypercalcemia due to PHPT. Immediate surgery was not feasible because the patients had severe systemic illness, such as seizures and altered sensorium (case 1); acute severe pancreatitis (cases 2 and 3); or coronavirus disease 2019 pneumonia (case 4). Intravenous normal saline and parenteral salmon calcitonin were inadequate for controlling hypercalcemia. Intravenous bisphosphonates were avoided because of severe systemic illness in all cases and impaired renal function in three cases. Denosumab was administered to control hypercalcemia and allow the stabilization of patients for definitive surgical management. Following denosumab administration, serum calcium levels normalized, and general condition improved in all patients. Three patients underwent parathyroidectomy after two weeks and another patient after eight weeks. The use of denosumab for the management of severe hypercalcemia due to PHPT is efficacious and safe in patients when immediate surgical management is not feasible due to severe systemic illness.
MeSH term(s)	COVID-19 ; Calcium ; Denosumab/therapeutic use ; Humans ; Hypercalcemia/drug therapy ; Hypercalcemia/etiology ; Hyperparathyroidism, Primary/complications ; Hyperparathyroidism, Primary/drug therapy ; Hyperparathyroidism, Primary/surgery
Chemical Substances	Denosumab (4EQZ6YO2HI) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-09-29
Publishing country	Brazil
Document type	Case Reports
ISSN	2359-4292
ISSN (online)	2359-4292
DOI	10.20945/2359-3997000000408
Database	MEDical Literature Analysis and Retrieval System OnLINE

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