Dyslipidemia

Mancini, G.B. John; Hegele, Robert A.; Leiter, Lawrence A.

doi:10.1016/j.jcjd.2017.10.019

Cited by 58 publications

(33 citation statements)

References 111 publications

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“…Trials have shown a reduction of CVE in diabetic patients with use of statins including the Heart Protection Study which reported a 22% reduction in CVE including ischemic stroke[32] and The Collaborative Atorvastatin Diabetes Study[33,34] which reported a 37% reduction in the primary end point of CVE also including ischemic stroke. Meta-analysis of 14 randomized clinical trials including over 18000 patients showed statin therapy reduced CVE by 21% and vascular mortality by 13% for every 39 mg/dL decrease in LDL-C during an average follow up of 4.3 years[34,35].…”

Section: Therapeutic Strategiesmentioning

confidence: 99%

Management of diabetic dyslipidemia: An update

Jialal

Singh

2019

WJD

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Diabetic dyslipidemia is a cluster of lipoprotein abnormalities characterized by increased triglyceride level, decreased high-density lipoprotein-cholesterol levels and increase in small dense low-density lipoprotein (LDL) particles. It is extremely common in type 2 diabetes (T2DM) affecting around 70 % of patients. Diabetic is a significant risk factor for atherosclerotic cardiovascular disease (ASCVD) which is the most common cause of death in the United States and LDL-cholesterol is the number 1 predictor of ASCVD events in T2DM. The purpose of this review is to discuss the pathophysiology and treatment of diabetic dyslipidemia. In this review, we have discussed both non-pharmacological and pharmacological treatment modalities including major treatment trials which have impacted the cardiovascular outcomes in patients with diabetes. Statin therapy is the mainstay of treatment to reduce ASCVD by decreasing LDL-C by 30%-49% or at least 50% depending on risk level. Attractive adjunctive therapies include Ezetimibe which is more cost effective and PCSK9 inhibitors which display potent LDL-cholesterol lowering and ASCVD event reduction. For severe hypertriglyceridemia, to avert the risk of pancreatitis, both fish oil and fenofibrate in concert with diet is the best strategy.

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Section: Therapeutic Strategiesmentioning

confidence: 99%

Management of diabetic dyslipidemia: An update

Jialal

Singh

2019

WJD

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“…Alternatively, self-reported or physician-reported diagnosis, hospital database diagnosis, or specifically reported prediabetes-related medication or intervention use may be used as a marker of prediabetes.Overweight or obesity is defined using body mass index (BMI) z-score on 85–94.9th percentile indicating overweight and ≥ 95th percentile for obesity in children [46] and BMI 25–29.9 kg/m 2 indicating overweight and ≥ 30 kg/m 2 indicating obesity in adults [47]. Dyslipidemia is assessed by detecting abnormal levels of total cholesterol, high-density lipoprotein cholesterol, triglycerides, low-density lipoprotein cholesterol (measured or calculated), non-high-density lipoprotein cholesterol, or apolipoprotein A and B measured in, or converted to, mmol/L [48]. Hypertension is defined in children as systolic and/or diastolic blood pressure (BP) ≥ 95th percentile according to age- and sex-specific BP centiles and reported in millimeters of mercury (mmHg) [49].…”

Section: Methodsmentioning

confidence: 99%

“…Dyslipidemia is assessed by detecting abnormal levels of total cholesterol, high-density lipoprotein cholesterol, triglycerides, low-density lipoprotein cholesterol (measured or calculated), non-high-density lipoprotein cholesterol, or apolipoprotein A and B measured in, or converted to, mmol/L [48].…”

Section: Methodsmentioning

confidence: 99%

The impact of environmental cadmium exposure on type 2 diabetes risk: a protocol for an overview of systematic reviews

et al. 2019

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BackgroundType 2 diabetes mellitus (T2DM) is a worldwide epidemic, and while its etiology is polygenic, the role of environmental contaminant exposure in T2DM pathogenesis is of increasing importance. However, the evidence presented in systematic reviews on the relationship between cadmium exposure and T2DM development is inconsistent. This overview aims to assess existing evidence from systematic reviews linking cadmium exposure to T2DM and select metabolic disorders in humans.MethodsSearches will be conducted in Medline, Embase, Web of Science, GEOBASE, BIOSIS Previews, and Cochrane Database of Systematic Reviews. Two reviewers (J.H and S.T.) will independently complete screening, data abstraction, risk of bias evaluation, and quality assessment. The primary outcome will be the association between cadmium exposure and T2DM prevalence. Secondary outcomes will include prediabetes, obesity, dyslipidemia, hypertension, and non-alcoholic fatty liver disease. We will perform a meta-analysis if two or more studies assess similar populations, utilize analogous methods, have related study designs, and evaluate similar outcomes.DiscussionThis overview will assess current evidence from systematic reviews for the association between cadmium exposure and risk of T2DM and other metabolic morbidities. This overview may be helpful for policy-makers and healthcare teams aiming to mitigate T2DM risk in populations at risk of cadmium exposure.Systematic review registrationPROSPERO CRD42019125956

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“…While chronic hyperglycemia is one of the main risk factors for developing DN 2 , multiple clinical trials showed that insulin resistance, a common characteristic of type 2 diabetes, is an independent risk factor in developing chronic kidney disease 3 . Dyslipidemia in diabetic patients is commonly characterized by elevated circulating levels of free fatty acids (FFA) and triglycerides (hypertriglyceridemia) 4 . The lipotoxicity due to elevated FFA levels is a major factor and a key contributor to insulin resistance including the kidney 5 , 6 .…”

Section: Introductionmentioning

confidence: 99%

Saturated fatty acids induce insulin resistance in podocytes through inhibition of IRS1 via activation of both IKKβ and mTORC1

Denhez

Rousseau

Spino

et al. 2020

Sci Rep

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Diabetic nephropathy (DN), a microvascular complication of diabetes, is the leading cause of end-stage renal disease worldwide. Multiple studies have shown that podocyte dysfunction is a central event in the progression of the disease. Beside chronic hyperglycemia, dyslipidemia can induce insulin resistance and dysfunction in podocytes. However, the exact mechanisms of free fatty acid (FFA)-induced podocyte insulin unresponsiveness are poorly understood. We used a type 2 diabetic mouse model (db/db) and mouse podocytes exposed to palmitic acid for 24 h followed by an insulin stimulation. Renal function and pathology were evaluated at 25 weeks of age to confirm the DN development. Our results demonstrate that saturated FFA activated the serine/threonine kinases IκB kinase (IKK)β/IκBα and mTORC1/S6K1, but not protein kinase C and c-jun N-terminal kinase, in podocytes and glomeruli of db/db mice. Activation of both kinases promoted serine 307 phosphorylation of IRS1, a residue known to provoke IRS1 inhibition. Using IKK, mTORC1 and ceramide production inhibitors, we were able to blunt IRS1 serine 307 phosphorylation and restore insulin stimulation of Akt. In conclusion, our results indicate that FFA and diabetes contribute to insulin resistance through the activation of IKKβ and S6K1 leading to podocyte dysfunction and DN.

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Dyslipidemia

Cited by 58 publications

References 111 publications

Management of diabetic dyslipidemia: An update

Management of diabetic dyslipidemia: An update

The impact of environmental cadmium exposure on type 2 diabetes risk: a protocol for an overview of systematic reviews

Saturated fatty acids induce insulin resistance in podocytes through inhibition of IRS1 via activation of both IKKβ and mTORC1

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