Chronic Kidney Disease-Induced Insulin Resistance: Current State of the Field

Dave, Natasha; Wu, Jiao; Thomas, Sandhya S.

doi:10.1007/s11892-018-1010-8

Cited by 29 publications

(20 citation statements)

References 63 publications

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“…High calorie dietary habits coupled with low levels of physical activity are the primary cause of metabolic syndrome in today’s world. IR is a key risk factor in the pathogenesis of various chronic diseases, including T2DM, chronic kidney disease and cognitive disorders [19,20,21]. Natural products are thought to be important sources for anti-T2DM drug discovery [22].…”

Section: Discussionmentioning

confidence: 99%

Theaflavins Improve Insulin Sensitivity through Regulating Mitochondrial Biosynthesis in Palmitic Acid-Induced HepG2 Cells

et al. 2018

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Theaflavins, the characteristic and bioactive polyphenols in black tea, possess the potential improving effects on insulin resistance-associated metabolic abnormalities, including obesity and type 2 diabetes mellitus. However, the related molecular mechanisms are still unclear. In this research, we investigated the protective effects of theaflavins against insulin resistance in HepG2 cells induced by palmitic acid. Theaflavins significantly increased glucose uptake of insulin-resistant cells at noncytotoxic doses. This activity was mediated by upregulating the total and membrane bound glucose transporter 4 protein expressions, increasing the phosphor-Akt (Ser473) level, and decreasing the phosphorylation of IRS-1 at Ser307. Moreover, theaflavins were found to enhance the mitochondrial DNA copy number, down-regulate the PGC-1β mRNA level and increase the PRC mRNA expression. Mdivi-1, a selective mitochondrial division inhibitor, could attenuate TFs-induced promotion of glucose uptake in insulin-resistant HepG2 cells. Taken together, these results suggested that theaflavins could improve hepatocellular insulin resistance induced by free fatty acids, at least partly through promoting mitochondrial biogenesis. Theaflavins are promising functional food ingredients and medicines for improving insulin resistance-related disorders.

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Section: Discussionmentioning

confidence: 99%

Theaflavins Improve Insulin Sensitivity through Regulating Mitochondrial Biosynthesis in Palmitic Acid-Induced HepG2 Cells

et al. 2018

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“…[40][41][42] On the other side, some studies also observed increased IR states could be regulated via overactivated inflammatory response in the patients with CKD. [43][44][45][46][47] These results suggested there might be an internal relationship between IR and mildly decreased eGFR. For now, there were few studies focused on the mild decline of eGFR, but some results from CKD could indirectly confirm our conclusion.…”

Section: Open Accessmentioning

confidence: 99%

Usefulness of metabolic score for insulin resistance index in estimating the risk of mildly reduced estimate glomerular filtration rate: a cross-sectional study of rural population in China

Wang

Guo

et al. 2021

BMJ Open

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ObjectivesThis study aimed to reveal the association between metabolic score for insulin resistance (MetS-IR) and the risk of mildly decreased estimated glomerular filtration rate (eGFR), and explore the evaluation effect of MetS-IR on the progress of eGFR decline.Study designA cross-sectional study.Setting and participantsA total of 11 956 rural participants (aged ≥35 years) from northeastern China were enrolled in the study. After excluding the subjects whose data were not integrated or who met the exclusion criteria, we finally obtained 11 042 participants in the present study.Main outcome measuresMildly decreased eGFR was defined as 60–90 mL/min/1.73 m2.ResultsThe prevalence of mildly decreased eGFR in the general population was 36.9%. After adjustment of covariates, each SD increment of MetS-IR could bring 26.3% additional risk of mildly decreased eGFR (OR: 1.263, 95% CI: 1.066 to 1.497, p=0.007). When MetS-IR was classified into four levels by quartile, we observed participants in the top level had 3.032-fold risk of mildly decreased eGFR (OR: 3.032, 95% CI: 1.841 to 4.991, p<0.001) compared with those from the bottom level. Further, we found the participants with higher MetS-IR score were more likely to aggravate into a worse renal state which presented as higher risk of accelerated decline of eGFR, by additional 28.3% risk in whole participants (OR: 1.283, 95% CI: 1.150 to 1.430, p<0.001) and 41.9% in men (OR: 1.419, 95% CI: 1.183 to 1.701, p<0.001).ConclusionHigh MetS-IR was associated with high risk of mildly reduced eGFR and often accompanied by a high risk of accelerated decline in eGFR. Hence, we believed MetS-IR was a suitable indicator to evaluate the risk of early-stage renal dysfunction.

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“…On the other hand, insulin resistance develops in patients with renal failure. 16 It is thought that insulin resistance also contributed to the etiopathogenesis of diabetes in our patient, who was obese and had renal dysfunction.…”

Section: Discussionmentioning

confidence: 70%

A case of familial recurrent 17q12 microdeletion syndrome presenting with severe diabetic ketoacidosis

Aydın¹,

Kıral²,

Susam³

et al. 2022

Turk J Pediatr

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Background. Heterozygous intragenic mutations of the hepatocyte nuclear factor 1 homeobox b gene (HNF1B) located on chromosome 17 and microdeletion of 17q12 region (17q12MD) leads to the complete loss of this gene, which causes renal cystic disease, diabetes mellitus (MODY5), hypomagnesemia, hyperuricemia, liver enzyme abnormalities, genital tract abnormalities and exocrine pancreatic insufficiency. In addition, patients with 17q12MD also have facial dysmorphism, neuro-developmental and neuropsychiatric disorders. Case. A 16-year-old girl with obesity and mild facial dysmorphism was admitted to the hospital with symptoms of diabetes that started two days prior to her admission. She was diagnosed with severe diabetic ketoacidosis and treated accordingly. She had been followed up with the diagnoses of multicystic renal disease, hydronephrosis, hepatosteatosis, hypomagnesemia and hyperuricemia since the age of six. She had mild intellectual disability. Her menarche started two months ago. Cranial magnetic resonance imaging revealed mild diffuse cerebral and cerebellar atrophy and a partial empty sella. Her mother had diabetes, hypomagnesemia and mild intellectual disability and her maternal grandfather and uncle had diabetes. Her grandfather also had renal cystic disease. All of them are on oral antidiabetic medication. The genetic analysis of the patient and her mother revealed a loss of 1.6 megabases in chromosome 17q12. Conclusions. MODY5 should be kept in mind in patients with diabetes who present with extra pancreatic findings, especially with renal cystic disease, more over, a genetic analysis including the study of 17q12MD should be carried out in patients who present with additional neuropsychiatric findings. Ketoacidosis can be seen in patients with MODY5. Ketoacidosis and renal anomalies and dysfunction are factors that increase and affect the severity of each other in these patients.

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Chronic Kidney Disease-Induced Insulin Resistance: Current State of the Field

Cited by 29 publications

References 63 publications

Theaflavins Improve Insulin Sensitivity through Regulating Mitochondrial Biosynthesis in Palmitic Acid-Induced HepG2 Cells

Theaflavins Improve Insulin Sensitivity through Regulating Mitochondrial Biosynthesis in Palmitic Acid-Induced HepG2 Cells

Usefulness of metabolic score for insulin resistance index in estimating the risk of mildly reduced estimate glomerular filtration rate: a cross-sectional study of rural population in China

A case of familial recurrent 17q12 microdeletion syndrome presenting with severe diabetic ketoacidosis

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