Diabetic dyslipidaemia: from basic research to clinical practice*

By Marja-Riitta Taskinen. Diabetologia, 2003

911 citations recorded by the source corpus.

Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Surgery

View Paper: https://www.semanticscholar.org/paper/2594dc8cddbcdf7e641c7da5b81dd5ccde6294f8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. B. Vergès
2. Martin Adiels
3. S. Olofsson
4. J. Despres
5. André Tchernof
6. M. Matsuda
7. I. Shimomura
8. Jan Boren

In Endocrinology, Diabetes and Metabolism

1. André Tchernof
2. B. Vergès
3. J. Despres
4. Martin Adiels
5. S. Olofsson
6. I. Shimomura
7. M. Matsuda
8. Jan Boren

In Surgery

1. B. Vergès
2. Martin Adiels
3. S. Olofsson
4. André Tchernof
5. J. Despres
6. I. Shimomura
7. M. Matsuda
8. Jan Boren

Citations in the corpus

• ATVB In Focus Metabolic Syndrome and Atherosclerosis (2008, background): “Subjects diagnosed with the metabolic syndrome display, most noticeably, an increased production of VLDL (1), and there is a reduction in the catabolic rate of apoB-containing lipoproteins, in particular IDL and LDL (2).”
• Increased oxidative stress in obesity: implications for metabolic syndrome, diabetes, hypertension, dyslipidemia, atherosclerosis, and cancer. (2013, background): “[87] Taskinen MR.”
• Atherosclerotic Cardiovascular Disease and Heart Failure in Type 2 Diabetes – Mechanisms, Management, and Clinical Considerations (2016, neutral): “The transfer of triglycerides from triglyceride-rich lipoproteins to HDL and LDL cholesterol is facilitated by cholesteryl ester transfer protein (CETP).(111,112) Hypertriglyceridemia stimulates CETP activity, resulting in HDL and LDL cholesterol with high triglyceride content.”
• Pathophysiology of human visceral obesity: an update. (2013, background): “However, insulin has a blunted ability to inhibit VLDL secretion in visceral obesity, leading to increased VLDL secretion and hypertriglyceridemia (545, 546, 634).”
• Overproduction of large VLDL particles is driven by increased liver fat content in man (2006, background): “VLDL1 particles are converted in the circulation by cholesteryl ester transport protein and hepatic lipase – which are commonly increased in type 2 diabetes – to small atherogenic LDL particles [1].”
• Pathophysiology of diabetic dyslipidaemia: where are we? (2015, background): “Increased plasma triacylglycerol levels in patients with type 2 diabetes are largely due to an increased number of VLDLs, particularly large VLDL1 particles [6].”
• Pathophysiology of Type 2 Diabetes Mellitus (2020, background): “hyperinsulinemia, abnormalities in adipokines and adipocytokines have been implicated [190].”