Managing diabetes and liver disease association

Hamed, Abd Elkhalek; Elsahar, Medhat; Elwan, Nadia; El‐Nakeep, Sarah; Naguib, Mervat; Soliman, Hanan; Aboubakr, Ashraf; AbdelMaqsod, Amany; Sedrak, Heba; Assaad, Samir N.; Elwakil, Reda; Esmat, Gamal; Salh, Samira; Mostafa, Taymour; Mogawer, Sherif; Sadek, Sameh Emil; Saber, Maha M.; Ezelarab, Hanan; Mahmoud, Asem Ashraf; Sultan, Souad; Kassas, Mohamed El; Kamal, Ehab; Elsayed, Naglaa M.; Moussa, Shorouk

doi:10.1016/j.ajg.2018.08.003

Cited by 34 publications

(53 citation statements)

References 210 publications

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“…[16] It does not undergo hepatic metabolism and is excreted unchanged by tubular secretion and glomerular filtration in the urine. [38]…”

Section: Methodsmentioning

confidence: 99%

“…[38] Lactic acidosis can occur through two mechanisms. Metformin shifts intracellular oxidation-reduction potential toward anaerobic metabolism augmenting lactate production.…”

Section: Methodsmentioning

confidence: 99%

“…Nevertheless, there may be an enhanced risk of developing lactic acidosis in the clinical setting of impaired liver function. [38] It is estimated that incidence of lactic acidosis is 0.03–0.5 cases/1000 patient-years in metformin-treated population. However, the incidence of lactic acidosis among patients with T2DM who consume metformin does not differ from the incidence in T2DM patients not receiving metformin.…”

Section: Methodsmentioning

confidence: 99%

“…[38] A review by Khan et al . suggested that if a patient has stable CLD and few other comorbidities, metformin is likely to be reasonably safe, but the dose should be decreased to a maximum of 1500 mg daily, and the drug should be withdrawn if liver or renal function is deteriorating, or in the setting of acute illness or decompensation.…”

Section: Methodsmentioning

confidence: 99%

“…[54] NASH can also be associated with impaired defense in countering hypoglycemia. [3852] CLD patients who are malnourished are at higher risk of hypoglycemia. [15] Alcohol-induced enzyme degradation of SUs in patients with alcoholic liver disease may manifest decreased clinical effectiveness of SUs.…”

Section: Methodsmentioning

confidence: 99%

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Consensus statement on dose modifications of antidiabetic agents in patients with hepatic impairment

Gangopadhyay

Singh

2017

Indian J Endocr Metab

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Liver disease is an important cause of mortality in type 2 diabetes mellitus (T2DM). It is estimated that diabetes is the most common cause of liver disease in the United States. Virtually, entire spectrum of liver disease is seen in T2DM including abnormal liver enzymes, nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, and acute liver failure. The treatment of diabetes mellitus (DM) in cirrhotic patients has particular challenges as follows: (1) about half the patients have malnutrition; (2) patients already have advanced liver disease when clinical DM is diagnosed; (3) most of the oral antidiabetic agents (ADAs) are metabolized in the liver; (4) patients often have episodes of hypoglycemia. The aim of this consensus group convened during the National Insulin Summit 2015, Puducherry, was to focus on the challenges with glycemic management, with particular emphasis to safety of ADAs across stages of liver dysfunction. Published literature, product labels, and major clinical guidelines were reviewed and summarized. The drug classes included are biguanides (metformin), the second- or third-generation sulfonylureas, alpha-glucosidase inhibitors, thiazolidinediones, dipeptidyl peptidase-4 inhibitors, sodium-glucose co-transporter 2 inhibitors, glucagon-like peptide-1 receptor agonists, and currently available insulins. Consensus recommendations have been drafted for glycemic targets and dose modifications of all ADAs. These can aid clinicians in managing patients with diabetes and liver disease.

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“…[16] It does not undergo hepatic metabolism and is excreted unchanged by tubular secretion and glomerular filtration in the urine. [38]…”

Section: Methodsmentioning

confidence: 99%

“…[38] Lactic acidosis can occur through two mechanisms. Metformin shifts intracellular oxidation-reduction potential toward anaerobic metabolism augmenting lactate production.…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Consensus statement on dose modifications of antidiabetic agents in patients with hepatic impairment

Gangopadhyay

Singh

2017

Indian J Endocr Metab

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Protective Effects of Sepia Ink Melanin on Hepatic Tissue in Streptozotocin-Induced Diabetic Mice

Wang

Han²,

Dong³

et al. 2022

J. Ocean Univ. China

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Attenuation of Hyperglycemia in Diabetic Rats Assisted by Immobilized Probiotic in Sodium Alginate

Arriaga-Morales,

Ordaz-Pichardo,

Castro‑Muñoz

et al. 2023

Probiotics & Antimicro. Prot.

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Diabetes mellitus type 2 (DM2) is the most common chronic disease worldwide, characterized mainly by increased glucose concentration in the blood and affecting several organs’ functionality. The daily consumption of probiotic bacteria can help control diabetes and reduce the damage caused. Cell immobilization techniques are a powerful tool that provides physical cell protection to such probiotic bacteria against gastrointestinal conditions. We suggest that cell immobilization could be a significant vector for delivering a high quantity of viable probiotics to the gut, helping attenuate hyperglycemia in diabetic rats. Seventy male Wistar rats were used in this work. Nicotinamide was administrated via intraperitoneal injection 15 minutes before inducing type 2 diabetes (DM2), followed by a second intraperitoneal injection of streptozotocin to induce DM2. Rats were divided into seven groups. For 45 days, a specific treatment was applied to each group. The group of rats, supplied with immobilized Lactobacillus casei, showed a serum glucose concentration of 137 mg/dL, which was close to the one observed in the groups of healthy rats (117 mg/dL) and rats treated with metformin (155 mg/dL). The diabetic rats without treatment presented a higher serum glucose concentration (461 mg/dL). In the rats treated with immobilized L. casei, there was no biochemical parameter alteration, and the cell morphology of the analyzed tissues was similar to those of the healthy group. The consumption of immobilized L. casei could allow a high quantity of viable probiotics to be delivered to the gut, reducing serum glucose concentration by up to 70% compared to diabetic rats and reducing organ damage caused by diabetes.

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Managing diabetes and liver disease association

Cited by 34 publications

References 210 publications

Consensus statement on dose modifications of antidiabetic agents in patients with hepatic impairment

Consensus statement on dose modifications of antidiabetic agents in patients with hepatic impairment

Protective Effects of Sepia Ink Melanin on Hepatic Tissue in Streptozotocin-Induced Diabetic Mice

Attenuation of Hyperglycemia in Diabetic Rats Assisted by Immobilized Probiotic in Sodium Alginate

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