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Book: Type 2 diabetes and the evolving paradigm in glucose regulation

Abdul-Ghani, Muhammad A.

(The American journal of managed care ; 19,3, Suppl.)

2013

Title variant	Type-2-diabetes and the evolving paradigm in glucose regulation
Author's details	[Muhammad A. Abdul-Ghani]
Series title	The American journal of managed care ; 19,3, Suppl.
Collection
Language	English
Size	S. S41 - S52 : graph. Darst.
Publisher	Managed Care & Healthcare Communications
Publishing place	S.l.
Publishing country	United States
Document type	Book
HBZ-ID	HT017599178
Database	Catalogue ZB MED Medicine, Health

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Shelf mark	Loan status	Location
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Article ; Online: Fasting Hyperinsulinemia and Obesity: Cause or Effect.

Abdul-Ghani, Muhammad / DeFronzo, Ralph A

The Journal of clinical endocrinology and metabolism

2023 Volume 108, Issue 10, Page(s) e1151–e1152

MeSH term(s)	Humans ; Insulin Secretion ; Mendelian Randomization Analysis ; Hyperinsulinism/complications ; Obesity/complications ; Fasting ; Body Fat Distribution ; Insulins
Chemical Substances	Insulins
Language	English
Publishing date	2023-03-28
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad118
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Article ; Online: Insulin Resistance and Hyperinsulinemia: the Egg and the Chicken.

Abdul-Ghani, Muhammad / DeFronzo, Ralph A

The Journal of clinical endocrinology and metabolism

2021 Volume 106, Issue 4, Page(s) e1897–e1899

MeSH term(s)	Animals ; Chickens ; Humans ; Hyperinsulinism ; Insulin ; Insulin Resistance
Chemical Substances	Insulin
Language	English
Publishing date	2021-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgaa364
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Article: Sodium-Glucose Cotransporter 2 Inhibitors and the Kidney.

DeFronzo, Ralph A / Abdul-Ghani, Muhammad

Diabetes spectrum : a publication of the American Diabetes Association

2021 Volume 34, Issue 3, Page(s) 225–234

Abstract: Diabetic kidney disease (DKD) accounts for about half of individuals entering end-stage renal disease programs. Patients with DKD frequently have associated microvascular complications and are at very high risk for developing macrovascular complications. ...

Abstract	Diabetic kidney disease (DKD) accounts for about half of individuals entering end-stage renal disease programs. Patients with DKD frequently have associated microvascular complications and are at very high risk for developing macrovascular complications. Comprehensive treatment involves slowing or preventing the decline in glomerular filtration rate (GFR) and preventing macrovascular and further microvascular complications. Maintaining an A1C <6.5% represents primary prevention; in established DKD, tight blood pressure control is essential. ACE inhibitors/angiotensin receptor blockers (ARBs) and sodium-glucose cotransporter 2 (SGLT2) inhibitors can be used in combination to slow the rate of decline in GFR. This article reviews the general approach to DKD treatment and summarizes renal outcomes in four cardiovascular outcomes trials of SGLT2 inhibitors. Together, these trials provide conclusive evidence that SGLT2 inhibitors, added to an ACE inhibitor or ARB, slow the progression of DKD.
Language	English
Publishing date	2021-08-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211544-4
ISSN	1040-9165
ISSN	1040-9165
DOI	10.2337/ds20-0071
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Article ; Online: Personalized approach for type 2 diabetes pharmacotherapy: where are we and where do we need to be?

Abdul-Ghani, Muhammad / DeFronzo, Ralph A

Expert opinion on pharmacotherapy

2021 Volume 22, Issue 16, Page(s) 2113–2125

Abstract: Introduction: Cluster analysis has identified distinct groups of type 2 diabetes (T2D) subjects with distinct metabolic characteristics. Thus, personalizing pharmacologic therapy to individual phenotypic and pathophysiologic characteristics has ... ...

Abstract	Introduction: Cluster analysis has identified distinct groups of type 2 diabetes (T2D) subjects with distinct metabolic characteristics. Thus, personalizing pharmacologic therapy to individual phenotypic and pathophysiologic characteristics has potential to improve metabolic control and reduce risk of microvascular and macrovascular complications. Areas covered: The authors review the classification of T2D, genetic markers, pathophysiology and natural history of T2D, the ABCDE approach to therapy, the ADA/EASD stepwise approach to therapy, available antidiabetic agents, and provide a more rational therapeutic approach based upon pathophysiology and cardiovascular and renal outcome trials. Expert opinion: Although insulin resistance is the earliest detectable abnormality, overt T2D does not occur in the absence of progressive beta cell failure. Because of the complex etiology of T2D (Ominous Octet), initiation of therapy with combined agents that (i) target both insulin resistance and beta cell dysfunction and (ii) prevent macrovascular, as well as microvascular, complications will be required. The ratio of C-peptide at 120 minutes (OGTT) to baseline C-peptide predicts with high sensitivity who will respond to metformin, the response to glucose-lowering agents and provides a useful tool to guide optimal glucose lowering therapy.
MeSH term(s)	Blood Glucose ; C-Peptide ; Diabetes Mellitus, Type 2/drug therapy ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulin ; Insulin-Secreting Cells
Chemical Substances	Blood Glucose ; C-Peptide ; Hypoglycemic Agents ; Insulin
Language	English
Publishing date	2021-08-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2001535-5
ISSN	1744-7666 ; 1465-6566
ISSN (online)	1744-7666
ISSN	1465-6566
DOI	10.1080/14656566.2021.1967319
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Article ; Online: Real-world effectiveness of sodium-glucose cotransporter-2 inhibitors on the progression of chronic kidney disease in patients without diabetes, with and without albuminuria.

Nakhleh, Afif / Abdul-Ghani, Muhammad / Gazit, Sivan / Gross, Adi / Livnat, Idit / Greenbloom, Maya / Yarden, Adva / Khazim, Khaled / Shehadeh, Naim / Melzer Cohen, Cheli

Diabetes, obesity & metabolism

2024

Abstract: Aim: To examine the renal effects of sodium-glucose cotransporter-2 (SGLT2) inhibition among non-diabetic individuals with chronic kidney disease (CKD) in a real-world setting.: Methods: We collected de-identified data on adults without diabetes and ... ...

Abstract	Aim: To examine the renal effects of sodium-glucose cotransporter-2 (SGLT2) inhibition among non-diabetic individuals with chronic kidney disease (CKD) in a real-world setting. Methods: We collected de-identified data on adults without diabetes and with an estimated glomerular filtration rate (eGFR) of 25-60 mL/min/1.73 m Results: Of a total of 354 participants with CKD, without diabetes, who received SGLT2 inhibitors and were followed for a median of 527 days, the mean age was 72.8 ± 11.8 years, 26% were female, and 91% used renin-angiotensin system blockade. The mean eGFR was 45.4 ± 9.5 mL/min/1.73 m Conclusion: In a real-world study of primarily older non-diabetic adults with CKD, SGLT2 inhibition was associated with a slower rate of kidney function decline, regardless of baseline UACR level.
Language	English
Publishing date	2024-04-28
Publishing country	England
Document type	Journal Article
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.15623
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Article ; Online: The impact of increased hepatic glucose production caused by empagliflozin on plasma glucose concentration in individuals with type 2 diabetes and nondiabetic individuals.

Abdelgani, Siham / Khattab, Ahmed / Adams, John / Baskoy, Gozde / Triplitt, Curtis / DeFronzo, Ralph A / Abdul-Ghani, Muhammad

Diabetes, obesity & metabolism

2023 Volume 26, Issue 3, Page(s) 1033–1039

Abstract: Aim: To examine the impact of increased hepatic glucose production (HGP) on the decrease in plasma glucose concentration caused by empagliflozin in individuals living with diabetes and in nondiabetic individuals.: Methods: A total of 36 individuals ... ...

Abstract	Aim: To examine the impact of increased hepatic glucose production (HGP) on the decrease in plasma glucose concentration caused by empagliflozin in individuals living with diabetes and in nondiabetic individuals. Methods: A total of 36 individuals living with diabetes and 34 nondiabetic individuals were randomized to receive, in double-blind fashion, empagliflozin or matching placebo in a 2:1 treatment ratio. Following an overnight fast, HGP was measured with 3- Results: On Day 1 of empagliflozin administration, the increase in urinary glucose excretion (UGE) in individuals with normal glucose tolerance was smaller than in those with impaired glucose tolerance and those living with diabetes, and was accompanied by an increase in HGP in all three groups. The amount of glucose returned to the systemic circulation as a result of the increase in HGP was smaller than that excreted by the kidney during the first 3 h after empagliflozin administration, resulting in a decrease in fasting plasma glucose (FPG) concentration. After 3 h, the increase in HGP was in excess of UGE, leading to a small increase in plasma glucose concentration, which reached a new steady state. After 12 weeks, the amount of glucose returned to the circulation due to the empagliflozin-induced increase in HGP was comparable with that excreted by the kidney in all three groups. Conclusion: The balance between UGE and increase in HGP immediately after sodium-glucose cotransporter-2 (SGLT2) inhibition determined the magnitude of decrease in FPG and the new steady state which was achieved. After 12 weeks, the increase in HGP caused by empagliflozin closely matched the amount of glucose excreted by the kidneys; thus, FPG level remained stable despite the continuous urinary excretion of glucose caused by SGLT2 inhibition.
MeSH term(s)	Humans ; Benzhydryl Compounds/therapeutic use ; Blood Glucose ; Diabetes Mellitus, Type 2/drug therapy ; Glucose/metabolism ; Glucosides ; Hypoglycemic Agents ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Benzhydryl Compounds ; Blood Glucose ; empagliflozin (HDC1R2M35U) ; Glucose (IY9XDZ35W2) ; Glucosides ; Hypoglycemic Agents ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2023-12-22
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.15404
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Article ; Online: Empagliflozin Reduces Liver Fat in Individuals With and Without Diabetes.

Abdelgani, Siham / Khattab, Ahmed / Adams, John / Baskoy, Gozde / Brown, Marissa / Clarke, Geoff / Larvenenko, Olga / DeFronzo, Ralph A / Abdul-Ghani, Muhammad

Diabetes care

2024 Volume 47, Issue 4, Page(s) 668–675

Abstract: Objective: To examine the effect of empagliflozin on liver fat content in individuals with and without type 2 diabetes (T2D) and the relationship between the decrease in liver fat and other metabolic actions of empagliflozin.: Research design and ... ...

Abstract	Objective: To examine the effect of empagliflozin on liver fat content in individuals with and without type 2 diabetes (T2D) and the relationship between the decrease in liver fat and other metabolic actions of empagliflozin. Research design and methods: Thirty individuals with T2D and 27 without were randomly assigned to receive in double-blind fashion empagliflozin or matching placebo (2:1 ratio) for 12 weeks. Participants underwent 75-g oral glucose tolerance testing and measurement of liver fat content with MRS before therapy and at study end. Hepatic glucose production before the start of therapy was measured with 3-3H-glucose. Results: Empagliflozin caused an absolute reduction of 2.39% ± 0.79% in liver fat content compared with an increase of 0.91% ± 0.64% in participants receiving placebo (P < 0.007 with ANOVA). The decrease in liver fat was comparable in both individuals with diabetes and those without (2.75% ± 0.81% and 1.93% ± 0.78%, respectively; P = NS). The decrease in hepatic fat content caused by empagliflozin was strongly correlated with baseline liver fat content (r = -0.62; P < 0.001), decrease in body weight (r = 0.53; P < 0.001), and improvement in insulin sensitivity (r = -0.51; P < 0.001) but was not related to the decrease in fasting plasma glucose or HbA1c or the increase in hepatic glucose production. Conclusions: Empagliflozin is effective in reducing liver fat content in individuals with and without T2D. The decrease in liver fat content is independent of the decrease in plasma glucose concentration and is strongly related to the decrease in body weight and improvement in insulin sensitivity.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2 ; Hypoglycemic Agents/therapeutic use ; Blood Glucose/metabolism ; Insulin Resistance ; Liver/metabolism ; Benzhydryl Compounds ; Body Weight ; Double-Blind Method ; Glucosides
Chemical Substances	Hypoglycemic Agents ; empagliflozin (HDC1R2M35U) ; Blood Glucose ; Benzhydryl Compounds ; Glucosides
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article
ZDB-ID	441231-x
ISSN	1935-5548 ; 0149-5992
ISSN (online)	1935-5548
ISSN	0149-5992
DOI	10.2337/dc23-1646
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Article ; Online: Type 2 diabetes subgroups and response to glucose-lowering therapy: Results from the EDICT and Qatar studies.

Abdul-Ghani, Tamam / Puckett, Curtiss / Migahid, Osama / Abdelgani, Siham / Migahed, Ayman / Adams, John / Triplitt, Curtis / DeFronzo, Ralph / Jayyousi, Amin / Abdul-Ghani, Muhammad

Diabetes, obesity & metabolism

2022 Volume 24, Issue 9, Page(s) 1810–1818

Abstract: Aim: To examine the efficacy of glucose-lowering medications in subgroups of patients with type 2 diabetes mellitus (T2DM).: Research design and methods: Cluster analysis was performed in participants in the Efficacy and Durability of Initial ... ...

Abstract	Aim: To examine the efficacy of glucose-lowering medications in subgroups of patients with type 2 diabetes mellitus (T2DM). Research design and methods: Cluster analysis was performed in participants in the Efficacy and Durability of Initial Combination Therapy for Type 2 Diabetes (EDICT) study and the Qatar study using age, body mass index (BMI), glycated haemoglobin (HbA1c), and homeostatic model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-β). Participants also underwent an oral glucose tolerance test with measurement of plasma glucose, insulin and C-peptide concentrations to derive independent measures of insulin secretion and insulin sensitivity. The response to glucose-lowering therapies (change in HbA1c) was measured in each participant cluster for 3 years. Results: Three distinct and comparable clusters/groups of T2DM patients were identified in both the EDICT and Qatar studies. Participants in Group 1 had the highest HbA1c and manifested severe insulin deficiency. Participants in Group 3 had comparable insulin sensitivity to those in Group 1 but better beta-cell function and better glucose control. Participants in Group 2 had the highest BMI with severe insulin resistance accompanied by marked hyperinsulinaemia, which was primarily attributable to decreased insulin clearance. Unexpectedly, participants in Group 1 had better response to combination therapy with pioglitazone plus exenatide than with insulin therapy or metformin sequentially followed by glipizide and basal insulin, while participants in Group 2 responded equally well to both therapies despite very severe insulin resistance. Conclusion: Distinct metabolic phenotypes characterize different T2DM clusters and differential responses to glucose-lowering therapies. Participants with severe insulin deficiency respond better to agents that preserve beta-cell function, while, surprisingly, patients with severe insulin resistance did not respond favourably to insulin sensitizers.
MeSH term(s)	Blood Glucose/metabolism ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Glucose/therapeutic use ; Glycated Hemoglobin A/metabolism ; Humans ; Hypoglycemic Agents/therapeutic use ; Insulin/metabolism ; Insulin Resistance ; Qatar/epidemiology
Chemical Substances	Blood Glucose ; Glycated Hemoglobin A ; Hypoglycemic Agents ; Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2022-06-29
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1454944-x
ISSN	1463-1326 ; 1462-8902
ISSN (online)	1463-1326
ISSN	1462-8902
DOI	10.1111/dom.14767
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Article ; Online: Type 2 diabetes and the evolving paradigm in glucose regulation.

Abdul-Ghani, Muhammad A

The American journal of managed care

2013 Volume 19, Issue 3 Suppl, Page(s) S43–50

Abstract: Type 2 diabetes mellitus (T2DM) is a multisystem disease comprising numerous metabolic defects that contribute to the development of hyperglycemia. Although insulin resistance in the skeletal muscle and liver together with progressive beta cell failure ... ...

Abstract	Type 2 diabetes mellitus (T2DM) is a multisystem disease comprising numerous metabolic defects that contribute to the development of hyperglycemia. Although insulin resistance in the skeletal muscle and liver together with progressive beta cell failure are traditionally thought of as the core defects responsible for the development and progression of hyperglycemia, research over the past 2 decades has revealed a far more complex interaction of organs and tissues, with consequences for the fundamental understanding of the mechanisms of glucose disequilibrium and the nature of T2DM itself. Dysfunctions in the gastrointestinal tract, adipose tissue, pancreatic alpha cells, brain, and kidneys have all been described, and together with insights into the involvement of liver, muscle, and beta cells produce a more robust picture of T2DM. The function of the kidneys in abnormal glucose homeostasis is a striking example of this evolution in T2DM knowledge, as the role of glucose transporters in regulating plasma glucose levels and producing hyperglycemia has enhanced current understanding of T2DM. As pathophysiologic mechanisms and defects continue to be discovered, they offer an expansion of potential targets for treatment of T2DM.
MeSH term(s)	Adipocytes/metabolism ; Appetite/physiology ; Brain/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Fasting ; Fatty Acids, Nonesterified/blood ; Gastric Inhibitory Polypeptide/blood ; Gastrointestinal Hormones/metabolism ; Glucagon/blood ; Glucagon-Like Peptide 1/deficiency ; Glucagon-Secreting Cells/metabolism ; Glucose/metabolism ; Humans ; Insulin Resistance/physiology ; Insulin-Secreting Cells/physiology ; Kidney/metabolism ; Liver/metabolism ; Muscle, Skeletal/metabolism ; Obesity/metabolism ; Obesity/physiopathology ; Sodium-Glucose Transport Proteins/metabolism
Chemical Substances	Fatty Acids, Nonesterified ; Gastrointestinal Hormones ; Sodium-Glucose Transport Proteins ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucagon (9007-92-5) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2013-02-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2035781-3
ISSN	1936-2692 ; 1088-0224 ; 1096-1860
ISSN (online)	1936-2692
ISSN	1088-0224 ; 1096-1860
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