Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                
Scribd
Upload
1 views

Research Introduction

Uploaded by

jsgswjtzpd
Copyright
© © All Rights Reserved
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
1 views

Research Introduction

Uploaded by

jsgswjtzpd
Copyright
© © All Rights Reserved
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
You are on page 1/ 3

INTRODUCTION

Diabetes mellitus is a group of metabolic diseases characterized by chronic hyperglycemia


resulting from defects in insulin secretion, insulin action, or both. Metabolic abnormalities in
carbohydrates, lipids, and proteins result from the importance of insulin as an anabolic
hormone.The main subtypes of DM are Type 1 diabetes mellitus (T1DM) and Type 2 diabetes
mellitus (T2DM) (1)
Excess fatty acids and proinflammatory cytokines are the cause of insulin resistance, which
impairs glucose transport and speeds up fat breakdown. The body responds by incorrectly raising
glucagon when there is an inadequate reaction to or production of insulin, which furthers the
development of hyperglycemia.(1)
Lipids, which include phospholipids, cholesterol, triglycerides (TG), and fatty acids, are thought
to be essential to the health of the human body because they serve as the building blocks of cell
membranes (phospholipids), are precursors to steroid hormones, bile acids, and vitamin D, and
are components of cell (2)
patients with T2DM frequently display an atherogenic lipid profile, which is characterized by
high plasma levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein
cholesterol (LDL-C), but low levels of HDL-C [3]; as well as increased free fatty acids and
increased small dense LDL (sdLDL), which significantly raises their risk for CVD through the
atherosclerosis process. Although hyperglycemia was linked to the development of
atherosclerotic lesions, dyslipidaemia, which resulted from the addition of increasing amounts of
cholesterol, was the primary driver of atherosclerosis progression independently of
hyperglycemia [4].
A growing body of research implies that dyslipidaemia is attributable to insulin resistance or
variables closely connected to insulin resistance, such as obesity, and that deteriorating
glycaemic control worsens lipid and lipoprotein abnormalities [5]. The fundamental causes of
this interaction may be increased proinflammatory adipokines and cytokines from larger adipose
tissue and increased free fatty acid flow brought on by insulin resistance [6].
Hyperglycemia and dyslipidemia together provide a more favorable atherogenic milieu in the
bloodstream, which quickens the development of atherosclerosis [7].

Lipid profile, including triglycerides and total, HDL, and LDL cholesterol, are modifiable factors
sensitive to obesity.
is a blood test that can measure the amount of cholesterol and triglycerides in your blood.
A cholesterol test can help determine your risk of the buildup of fatty deposits (plaques) in your
arteries that can lead to narrowed or blocked arteries throughout your body (atherosclerosis).
* Total cholesterol. This is a sum of your blood's cholesterol content.
* Low-density lipoprotein (LDL) cholesterol. This is called the "bad" cholesterol.
* High-density lipoprotein (HDL) cholesterol. This is called the "good" cholesterol because it
helps carry away LDL cholesterol,
* Triglycerides. Triglycerides are a type of fat in the blood. When you eat, your body converts
calories it doesn't need into triglycerides, which are stored in fat cells. High triglyceride levels
are associated with several factors, including being overweight, eating too many sweets or
drinking too much alcohol, smoking, being sedentary, or having diabetes with elevated blood
sugar levels.(8)

The 3 major components of the dyslipidemia of insulin resistance are increased triglyceride
levels, decreased high-density lipoprotein (HDL) cholesterol, and changes in the composition of
low-density lipoprotein (LDL) cholesterol. Hyperinsulinemia and the central obesity that
typically accompanies insulin resistance are thought to lead to overproduction of very low-
density lipoprotein (VLDL) cholesterol. The result is more triglyceride-rich particles, fewer HDL
particles, and more small, dense LDL. Postprandial triglyceride levels and measures of
postprandial remnants also may contribute to increased insulin resistance. Deficiency of
lipoprotein lipase, an insulin-sensitive enzyme, might explain the abnormal levels of remnant
particles in insulin resistance. (9,10)

REFRENCES
1) R.H. Unger, L. Orci Diabetes paracrinopathy and islet paracrinology. National Academy of Sciences of
the United States of America Proceedings. On September 14, 2010, [PubMed PMID: 20798346]A series
of metabolic illnesses known as diabetes mellitus are characterized by chronic hyperglycemia brought on
by deficiencies in insulin secretion, insulin action, or both. hypermetabolic conditions
10.3389/fendo.2013.00037. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
2) Sociedade Brasileira de Cardiologia. IV DiretrizBrasileira sobre Dislipidemias e Prevenção da
Aterosclerose. Departamento de Aterosclerose daSociedade Brasileira de Cardiologia. Arq Bras Cardiol.
2007;88 Suppl I:2-19.
3). Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult
treatment panel III). Executive summary of the third report of the National Cholesterol Education
Program (NCEP). Journal of the American Medical Association. 2001;285(19): 2486-2947. PubMed|
Google Scholar
4). Renard CB, Kramer F, Johansson F, Lamharzi N, Tannock LR, von Herrath MG et al. Diabetes and
diabetes-associated lipid abnormalities have distinct effects on initiation and progression of
atherosclerotic lesions. J Clin Invest. 2004;114(5): 659-668. PubMed| Google Scholar
5). Selvin E, Steffes MW, Zhu H, Matsushita K, Wagenknecht L, Pankow J et al. Glycated hemoglobin,
diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med. 2010 Mar 4;362(9): 800-11.
PubMed| Google Scholar
6) Chehade JM, Gladysz M, Mooradian AD. Dyslipidemia in type 2 diabetes: prevalence,
pathophysiology, and management. Drugs. 2013;73(4): 327-339. PubMed| Google Scholar
7). Regmi P, Gyawali P, Shrestha R, Sigdel M, Mehta KD, Majhi S. Pattern of dyslipidemia in type-2
diabetic subjects in Eastern Nepal. Journal for Nepal Association for Medical Laboratory Sciences.
2009;10(1): 11-13. Google Scholar
8)MedStar Research Institute, Washington, DC 20010, USA.
https://pubmed.ncbi.nlm.nih.gov/10418856/
9) Lee J.S., Chang P.Y., Zhang Y., Kizer J.R., Best L.G., Howard B.V. Triglyceride and HDL-C
Dyslipidemia and Risks of Coronary Heart Disease and Ischemic Stroke by Glycemic Dysregulation
Status: The Strong Heart Study. Diabetes Care. 2017;40:529–537. doi: 10.2337/dc16-1958. [PMC free
article] [PubMed] [CrossRef] [Google Scholar]
10). Rana J.S., Liu J.Y., Moffet H.H., Solomon M.D., Go A.S., Jaffe M.G., Karter A.J. Metabolic
dyslipidemia and risk of coronary heart disease in 28,318 adults with diabetes mellitus and low-density
lipoprotein cholesterol, 100 mg/dL. Am. J. Cardiol. 2015;116:1700–1704.
doi: 10.1016/j.amjcard.2015.08.039. [PubMed] [CrossRef] [Google Scholar]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6165005/

You might also like