EPIDEMIOLOGY:

An extensive data has confirmed the crucial role of dyslipidaemias in the pathogenesis of atherosclerotic coronary heart disease (CHD)^9-14. The randomly collected data from many studies have shown relation between blood lipid levels, dietary composition, prevalence (P) and incidence (I) of CHD¹⁵. During the past two decade, a various evidences of populations studies has confirmed that where the average serum cholesterol is high, the incidence (I) and prevalence (P) of CHD is also high^16,17. Several randomly collected data showed that few forms of adult dyslipidaemia are very common worldwide. Approximately half population had hypoalphalipoproteinemia (0.9mmol or 35mg/dL) and almost one-third of the population had fasting triglycerides above 2.26mmol (200mg/dL). The prevalence was higher in men, especially those over 50 years of age. Similar lipid abnormalities have been observed in certain ethnic groups such as Turks and in other Asian populations, including those in Bangladesh and Pakistan¹⁸. It was also seen that hypercholesterolemia was twice as frequent in US white males as compared to other ethnic groups. These observations suggested that the genetic as well as environmental factors may be responsible leading to hyperlipidaemia. Hypercholesterolemia was also found to be twice as common among white men in the United States as among other ethnic groups. These observations suggest that both genetic and environmental factors may contribute to hyperlipidaemia¹⁹.

Causes and Risk Factors of Hyperlipidaemia:

Many studies have clearly stated that the higher the level of LDL cholesterol, the greater the risk of cardiovascular diseases in both men and women of various ethnic and racial groups. In contrast, lower the level of HDL cholesterol, greater the risk of coronary heart diseases²⁰.

Fig. 2: Causes of hyperlipidemia²¹

Risk factors:

There is two types of risk factors in hyperlipidaemia:

I. Non modifiable risk factors

II. Modifiable risk factors

I. Non modifiable risk factors

Age and Gender: An unhealthy lifestyle is the main cause of hyperlipidaemia, but it can also be inherited by patients. When a man reaches his age 45 and a womanreaches her age 55, the risk of hyperlipidaemia naturally increases due to age^21-23. For women, this happens after menopause, when cholesterol levels tend to rise. Postmenopausal women haveelevated levels of total cholesterol, LDL-C, and apolipoprotein B compared topremenopausal women. Total HDL decreases in postmenopausal women^24-26.

Persistent sicknesses (Chronic diseases): Persistent sicknesses (Chronic diseases) that affect the cardiovascular framework can likewise cause elevated cholesterol levels. The conditions such as kidney issues and liver diseases, conditions that influence thyroid, a poor functions of the pituitary organ, and diabetescan also cause elevated cholesterol levels^25-27. High blood glucose adds to higher LDL cholesterol and lower HDL cholesterol²⁷.

II. Modifiable risk factors:

Physical latency and Smoking:

An exercise also tends to increase the good and reduce the bad cholesterol. Physical latency can prompt weight gain. Therefore physical latency is likewise considered a major risk component for hyperlipidaemia^28-30. Cigarette smoking harms the walls of the veins, making them liable to gather fatty deposits. Smoking may likewise bring down your degree of HDL. Absorption of nicotine prompts release of cortisol, growth hormone and catecholamine, activating adenylyl cyclase in fat tissue. This facilitates lipolysis leads to release of free fatty acids, results in production of VLDL and triglycerides^{31, 32}.

Medications:

Medications such asglucocorticoids and thiazides enhances the risk of dyslipidaemia³³.

Diet:

As per National Cholesterol Education Program (NCEP), healthy as well as good diet and losing weight brings down the bad cholesterol that gets stored in the body. A poor and unhealthy diet enhances the chances for occurrence ofhyperlipidaemia. Intake ofexcess cholesterol as well as fat contribute to elevatedlevels of lipid in theblood^33-38.

Lipoprotein Metabolism:

In the exogenous pathway, absorbed cholesterol and triglycerides (TGs) are transported in plasma as chylomicrons^{39, 40}. In the intestinal lumen, the dietary TGs is hydrolysed by a lipoprotein lipase into free fatty acids (FFAs) which move into the tissue and utilized^{41, 42}. The chylomicrons remnants (containing mainly cholesterol) pass to the liver where cholesterol is stored, oxidized to bile acids, or secreted in the bile. Alternatively, it may enter the synthesis of very low density lipoproteins (VLDL)^{43, 44}.

In the endogenous pathway, cholesterol and newly synthesized TGs are assembled as VLDL and delivered to the blood where TGsis hydrolysed by lipoprotein lipase into FFAs a described above^43-45. The smaller VLDL particles having less TGs and more cholesterol are now termed as low density lipoprotein (LDL). Cholesterol in the LDL may be:

1) Utilized by tissue

2) Returns again to the liver

3) Deposited in the blood vessels and cause atherosclerosis

When cells die, cholesterol in their plasma membranes is returned to the liver as plasma HDL particles. HDL functions as scavenger lipoproteins^45-48.

Table 2: Drugs used in hyperlipidaemia^48-50

Subclass	Drug	Mechanism of Action	Effects	Clinical Application	Toxicity
Statins	Atorvastatin, Simvastatin, Rosuvastatin,	Inhibit HMG-CoA reductase	Reduce cholesterol synthesis, reduction in triglycerides	Atherosclerosis, Acute coronary disease	Myopathy, Hepatic dysfunction
Fibrates	Fenofibrate, Gemfibrozil	Peroxisome proliferator activated receptor alpha (PPAR-a) agonist	Reduce release of very low density lipoproteins (VLDL), enhance lipoprotein lipase activity,	Hypertriglyceridemia	Myopathy, Hepatic dysfunction
Bile acidsequestrants	Colestipol, Cholestyramine	Binds bile acids in gut and prevents reabsorption	Reduces LDL	Elevated LDL, Digitalis toxicity	Constipation, Bloating
Sterol absorption inhibitors	Ezetimibe	Blocks sterol transporter NPC1L in brush order of intestine	Inhibits reabsorption of cholesterol excreted in bile	Elevated LDL	Hepatic dysfunction, Myositis
Niacin	Nicotinic acid	Reduces VLDL release from liver	Enhances HDL, reduces LDL & VLDL	Low HDL, elevated VLDL	Gastric irritation, Flushing
Pcsk9 humanized monoclonal antibodies	Evolocumab, Alirocumab	Complexes PCSK9	Inhibits catabolism of LDL receptor	Familial hypercholesterolemia	Nasopharyngitis, Flu like symptoms, rarely myalgia

Plant Bioactives and Extracts Used In Hyperlipidemia:

As per report of WHO, 70-80% of total population depends on conventional drugs from plant sources, for their essential medical care need⁵¹.A consistent technique, to prevent or to treat atherosclerosis and lessen the occurrence of cardiovascular infection occasions, is to target hyperlipidaemia by medicines or potentially dietary intercession⁵². The currentpharmacotherapy provide only symptomatic relief and are not free from any type of undesirable side effects. The goal, consequently, need to be discover newer drugs from plant kingdom which may offer cost effective therapeutic cure and would be free from undesirable side effects⁵³. With this point, efforts to make powerful and better anti-hyperlipidaemic drugs have led to discovery of normal natural products and have initiated the finding for new lipid-loweringagents from this source. Huge numbers of plants definitely stand out enough to be noticed in such manner and have been displayed to bring down plasma lipid levels⁵⁴.

Table 3: Literature review on the Plants investigated as Anti-hyperlipidemic agents^55-69

Sr. No.	Name of the Plant	Animal Model	Experimental animal	Extract/ Fraction	Parameters evaluated
1	Cassia auriculata L.	Streptozotocin induced diabetes	Male albino rats	Aqueous extract of leaves	TC, TG, HDL,LDL, VLDL, glucose
2	Carica papaya L.	Alloxan induced diabetes	Wistar albino rats of either sex	Aqueous extract of leaves	TC, TG, total protein , glucose
3	Brassica oleracea	Alloxan induced diabetes	White rabbits of both sexes	Methanolic extract of cabbages	TC,TG,HDL,LDL, glucose
4	Uvaria chamae	Streptozotocin induced diabetes	Albino rats of either sexes	Hydroethanolic extract of root	TC,TG,HDL,LDL, glucose
5	Siraitia grosvenorii	High-fat diet in combination with streptozotocin induced diabetes	Male C57BL/6 mice	Mogroside-rich extract (MGE)	TC,TG,HDL,LDL, glucose
6	Sophora falvescens	Poloxamer-407 induced and Cholesterol fed hyperlipidaemia	Male Sprague-Dawley rats	Methanolic extract of root and 4 fractions of (Kurarinol and Kuraridinol)	Total cholesterol (TC), tirgylcerides (TG), High density lipoprotein (HDL), Low density lipoprotein (LDL), Athero index (A.I.)
7	Pueraria thunbergiana	Triton WR1339 induced and High fat diet hyperlipidaemia	Male ICR mice	Kakkalide and Irisolidone isolated from flower	TC, TG
8	Panax notoginseng	High fat diet fed hyperlipidaemia	Male Sprague-Dawley rats	n-butanol extract of root	Serum TC, TG, LDL, Hepatic TC, TG
9	Glycine max L.	High fat diet (16% Lard oil) fed hyperlipidaemia	Male Sprague-Dawley rats	Anthocyanins isolated from seed coats	Body weight, adipose tissue weight, serum lipids
10	Ulmus davidiana	Triton WR1339 induced hyperlipidaemia	Male ICR mice	Glycoprotein	TC, TG, LDL, Antioxidant assays: Thiobarbituric acid reactive species (TBARS), etc.
11	Monascus fermented red mold dioscorea (RMD)	High cholesterol diet fed hyperlipidaemia	Male Golden Syrian hamsters	Dietary inclusion	TC, TG, HDL, LDL
12	Panax ginseng	Triton WR1339 and Corn oil induced hyperlipidaemia	Male ICR mice	Steamed and dried root of red ginseng (RG) and bifidodoterium fermented RG (FRG)	Serum TC, TG, postprandial blood glucose elevation
13	Ananas comosus L.	Fructose fed, High fat diet fed, Triton WR1339 induced hyperlipidaemia	Male ICR mice and Wistar rats	Ethanolic extract of leaves	Serum lipid profile, lipoprotein lipase activity, HMG CoA reductase activity
14	Ajuga iva L.	High cholesterol diet (1%) fed hyperlipidaemia	Male Wistar rats	Aqueous extract of whole plant	TC, TG, HDL, LDL, VLDL, TBARS
15	Dolichos biflorus L.	High fat diet fed hyperlipidaemia	Male Wistar rats	Methanolic extract of whole plant	TC, A.I., TC, TG, HDL, LDL

CONCLUSION:

It is quite evident from this review that the hyperlipidaemiaillness is significant gamble factor for cardiovascular illness. Hyperlipidaemia can be treated by recent synthetic therapeutic agents, healthy diet food and daily physical exercise. Assuming that mindful consideration is given to healthy diet maintenance and physical fitness might decrease the risk of cardiovascular and hyperlipidemic illness. Plant bioactives and extracts have a tremendous potential in the management of hyperlipidaemia, the challenge is to standardize these bioactives and extracts to ensure consistent efficacy as well as safety and also to subject these bioactives and extracts to testing with the evaluation of synthetic therapeutic agents. Evaluation of bioactive and extracts that have potential in treatment of hyperlipidaemia has provided significant interest in plant research.

ACKNOWLEDGMENT:

The authors would like to acknowledge Dr. Ashwini R. Madgulkar, Principal, AISSMS College of Pharmacy, Pune, for her encouragement and guidance.

CONFLICTS OF INTEREST:

No conflict of interest was declared by the authors. The authors alone are responsible for the content and writing of the paper.

REFERENCES:

1. Lin C-F, Chang Y-H, Chien S-C, Lin Y-H, Yeh H-Y. Epidemiology of dyslipidemia in the Asia Pacific region. International Journal of Gerontology. 2018;12(1):2–6.doi:https://doi.org/10.1016/j.ijge.2018.02.010

2. Frederickson DS, Lee RS. A system for phenotyping hyperlipidemia. Circulation 1965; 31:321-7.

3. Stone NJ. Secondary causes of Hyperlipidemia. Medical Clinics of North America. 1994;78(1):117–41.doi:https://doi.org/10.1016/S0025-7125(16)30179-1

4. Block ER, Edwards D. Effect of plasma membrane fluidity on serotonin transport by endothelial cells. American Journal of Physiology-Cell Physiology. 1987;253(5): 672-678. doi: 10.1152/ajpcell.1987.253.5.c672

5. Brunner LJ, Vadiei K, Luke DR. Cyclosporine disposition in the hyperlipidemic rat model. Research Community.1988; 59(3):339–348.

6. Steven Benowitz Associate Director of Communications ERP. Researchers finetune genomic links to high blood lipid levels [Internet]. Genome.gov. [cited 2022Dec28]. Available from: https://www.genome.gov/researchers-finetune-genomic-links-to-high-blood-lipid-levels

7. FREDRICKSON DONALDS. An international classification of hyperlipidemias and hyperlipoproteinemias. Annals of Internal Medicine. 1971;75(3):471.doi:10.7326/0003-4819-75-3-471

8. Shattat GF. A review article on Hyperlipidemia: Types, treatments and new drug targets. Biomedical and Pharmacology Journal. 2014;7(2):399–409.doi: 10.13005/bpj/504

9. Stamler J. Is relationship between serum cholesterol and risk of premature death from coronary heart disease continuous and graded? findings in 356,222 primary screenees of the Multiple Risk Factor Intervention Trial (MRFIT). JAMA: The Journal of the American Medical Association. 1986;256(20):2823–8.doi: 10.1001/jama.256.20.2823

10. Rose G, Shipley M. Plasma cholesterol concentration and death from coronary heart disease: 10 year results of the Whitehall Study. BMJ. 1986;293(6542):306–7.doi: 10.1136/bmj.293.6542.306

11. Gotto AM. Risk factor modification: Rationale for management of dyslipidemia. The American Journal of Medicine. 1998;104(2).doi: 10.1016/s0002-9343(98)00039-4

12. Castelli WP. Epidemiology of coronary heart disease: The framingham study. The American Journal of Medicine. 1984;76(2):4–12.doi: https://doi.org/10.1016/0002-9343(84)90952-5

13. Ramya KR, Batra K. Perception and knowledge of coronary heart disease among adolescents of Kerala. Asian Journal of Nursing Education and Research. 2015;5(3):327doi: 10.5958/2349-2996.2015.00067.1

14. Kaur S. A descriptive study to assess the prevalence of cardiovascular risk factors among adolescents in selected schools of Banga, district Shaheed Bhagat Singh Nagar, Punjab. Asian Journal of Nursing Education and Research. 2016;6(3):361.doi: 10.5958/2349-2996.2016.00068.9

15. Inkeles Stephen, Eisenberg Daniel. Hyperlipidaemia and coronary atherosclerosis. Medicine. 1981;60(2):110–23. doi:10.1097/00005792-198103000-00004

16. Kannel Williamb. Serum cholesterol, lipoproteins, and the risk of coronary heart disease. Annals of Internal Medicine. 1971;74(1):1. doi: 10.7326/0003-4819-74-1-1

17. Keys A. Coronary heart disease — the global picture. Atherosclerosis. 1975;22(2):149–92. doi: 10.1016/0021-9150(75)90001-5

18. Mahley RW, Palaoğlu KE, Atak Z, Dawson-Pepin J, Langlois AM, Cheung V, et al. Turkish heart study: Lipids, lipoproteins, and apolipoproteins. Journal of Lipid Research. 1995;36(4):839–59. doi:10.1016/s0022-2275(20)40067-7

19. Lavalle C, Alarcon-Segovia D, Del Giudice-Knipping JA, Fraga A. Association of Behçet's syndrome with HLA-B5 in the Mexican mestizo population. The Journal of Rheumatology. 1981;8(2):325-327. PMID: 7230164.

20. Steinberg D, Gotto, Jr AM. Preventing coronary artery disease by lowering cholesterol levels. JAMA. 1999;282(21):2043.doi: 10.1001/jama.282.21.2043

21. Abalkhail BA, Shawky S, Ghabrah TM, Milaat WA. Hypercholesterolemia and 5-year risk of development of coronary heart disease among university and school workers in Jeddah, Saudi Arabia. Preventive Medicine. 2000;31(4):390–5.doi: 10.1006/pmed.2000.0713

22. Sen A S A, Raju R. Comparative case control study on risk factors of coronary artery disease among sedentary and heavy workers. Asian Journal of Nursing Education and Research. 2021;:555–60.doi: 10.52711/2349-2996.2021.00130

23. Ogbeide DO, Karim A, Al-Khalifa IM, Siddique S. Population Based Study of Serum Lipid Levels in Al-Kharj Health Center, Saudi Arabia. Saudi MedicalJournal. 2004;25(12):1855-1857.

24. Al-Nozha MM, Arafah MR, Al-Mazrou YY, et al. Coronary artery disease in Saudi Arabia. Saudi Medical Journal. 2004;25(9):1165-1171. PMID: 15448760.

25. Saadi H, Carruthers SG, Nagelkerke N, Al-Maskari F, Afandi B, Reed R, et al. Prevalence of diabetes mellitus and its complications in a population-based sample in Al Ain, united arab emirates. Diabetes Research and Clinical Practice. 2007;78(3):369–77.doi: 10.1016/j.diabres.2007.04.008

26. Bonita R. Surveillance of risk factors for Noncommunicable Diseases: The WHO stepwise approach: Summary. Geneva: Noncommunicable Disease and Mental Health, World Health Organization; 2001.

27. WHO, EMRO, "stepwise WHO," 2005. - References - scientific research publishing. [Cited 2022Dec26]. Availablefrom:https://www.scirp.org/(S(351jmbntvnsjt1aadkposzje))/reference/referencespapers.aspx?referenceid=623427

28. Al-Moosa S, Allin S, Jemiai N, Al-Lawati J, Mossialos E. Diabetes and urbanization in the Omani population: An Analysis of National Survey Data. Population Health Metrics. 2006;4(1). doi: 10.1186/1478-7954-4-5

29. Bener A, Zirie M, Janahi IM, Al-Hamaq AOAA, Musallam M, Wareham NJ. Prevalence of diagnosed and undiagnosed diabetes mellitus and its risk factors in a population-based study of Qatar. Diabetes Research and Clinical Practice. 2009;84(1):99–106. doi: 10.1016/j.diabres.2009.02.003

30. Selvi JT, Shanthi Rosy J. A descriptive study to assess the knowledge and attitude of coronary artery disease risk factors among adults in Christian Mission Hospital at Madurai, Tamilnadu. International Journal of Nursing Education and Research. 2021;:262–4.doi: 10.52711/2454-2660.2021.00062

31. Jain RB, Ducatman A. Associations between smoking and lipid/lipoprotein concentrations among us adults aged ≥20 years. Journal of Circulating Biomarkers. 2018;7: 1849454418779310. doi:10.1177/1849454418779310

32. Gepner AD, Piper ME, Johnson HM, Fiore MC, Baker TB, Stein JH. Effects of smoking and smoking cessation on lipids and lipoproteins: Outcomes from a randomized clinical trial. American Heart Journal. 2011;161(1):145–51. doi: 10.1016/j.ahj.2010.09.023

33. Jackson RT, Al-Mousa Z, Al-Raqua M, Prakash P, Muhanna AN. Multiple coronary risk factors in healthy older Kuwaiti males. European Journal of Clinical Nutrition. 2002;56(8):709–14.doi: 10.1038/sj.ejcn.1601379.

34. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA: The Journal of the American Medical Association. 2001;285(19):2486–97.doi: 10.1001/jama.285.19.2486

35. Weinreich M, Frishman WH. Antihyperlipidemic therapies targeting PCSK9. Cardiology in Review. 2014;22(3):140–6.doi: 10.1097/crd.0000000000000014

36. Senthilkumar T, Tamilselvi A. Risk factors of cardiovascular disease in adolescents: A systematic review. Asian Journal of Nursing Education and Research. 2021;11(1):151–6.doi: 10.5958/2349-2996.2021.00039.2

37. Parvin SK, Devakirubai, Santha NJ, Selvarani G. Assessment of risk status for coronary artery disease in terms of selected risk factors among bus drivers. Asian Journal of Nursing Education and Research. 2020;10(3):291.doi: 10.5958/2349-2996.2020.00061.0

38. Murad S, Seema, Ghaffar A, Abbasi GM, Rehman IU, Qadir A. Abnormal lipid parameters and herbs. Asian Journal of Pharmaceutical Research. 2019;9(3):155.doi: 10.5958/2231-5691.2019.00024.8

39. Ramasamy I. Recent advances in physiological lipoprotein metabolism. Clinical Chemistry and Laboratory Medicine (CCLM). 2014;52(12).doi:10.1515/cclm-2013-0358

40. Hussain M. Intestinal lipid absorption and lipoprotein formation. Current Opinion in Lipidology. 2014;25(3):200–6.doi:10.1097/mol.0000000000000084

41. Iqbal J, & Hussain MM. Intestinal lipid absorption. American journal of physiology. Endocrinology and metabolism.2009; 296(6): E1183–E1194. doi:https://doi.org/10.1152/ajpendo.90899.2008

42. Wolska A, Dunbar RL, Freeman LA, Ueda M, Amar MJ, Sviridov DO, et al. Apolipoprotein C-II: New findings related to genetics, biochemistry, and role in triglyceride metabolism. Atherosclerosis. 2017;267:49–60.doi:10.1016/j.atherosclerosis.2017.10.025

43. Cooper AD. Hepatic uptake of Chylomicron remnants. Journal of Lipid Research. 1997;38(11):2173–92.doi:10.1016/s0022-2275(20)34932-4

44. Daniels TF, Killinger KM, Michal JJ, Wright Jr. RW, Jiang Z. Lipoproteins, cholesterol homeostasis and Cardiac Health. International Journal of Biological Sciences. 2009;:474–88.doi:10.7150/ijbs.5.474

45. Fisher E, Cohen D. Lipoprotein metabolism, dyslipidemia, and nonalcoholic fatty liver disease. Seminars in Liver Disease. 2013;33(04):380–8.doi:10.1055/s-0033-1358519

46. Willnow TE. Mechanisms of Hepatic Chylomicron remnant clearance. Diabetic Medicine. 1997;14(S3).doi:10.1002/(sici)1096-9136(199708)14:3+<s75::aid-dia449>3.0.co;2-9

47. Beisiegel U. Lipoprotein metabolism. European heart journal.1998;19 Suppl A: A20–A23.PMID: 9519338

48. Ebin.pub. Mansoura Clinical Pharmacology [2] [Internet]. ebin.pub. EBIN.PUB; 2016 [cited 2022Dec31]. Available from: https://ebin.pub/mansoura-clinical-pharmacology-2.html

49. Katzung B. Drugs used in dyslipidemia. In: Basic & Clinical Pharmacology. 14th ed. New York, California: McGraw-Hill Education; 2015. p. 626–41.

50. Tripathi KD. Hypolipidaemic drugs and plasma expanders. In: Essentials of Medical Pharmacology.7th ed. New Delhi: Jaypee Brothers Medical Publishers (p) Ltd; 2013. P. 634–46.

51. WHO establishes the Global Centre for Traditional Medicine in India [Internet]. World Health Organization. World Health Organization; 2022 [cited 2023Jan2]. Available from: https://www.who.int/news/item/25-03-2022-who-establishes-the-global-centre-for-traditional-medicine-in-india

52. Lapinleimu H, Salo P, Routi T, Lapinleimu H, Jokinen E, Välimäki I, et al. Prospective randomised trial in 1062 infants of diet low in saturated fat and cholesterol. The Lancet. 1995;345(8948):471–6.doi:https://doi.org/10.1016/S0140-6736(95)90580-4

53. Agarwal RC, Singh SP, Saran RK, Das SK, Sinha N, Asthana OP, Gupta PP, Nityanand S, Dhawan BN, Agarwal SS. Clinical trial of gugulipid--a new hypolipidemic agent of plant origin in primary hyperlipidemia. The Indian journal of medical research.1986; 84: 626–634.PMID: 3552974

54. Lee I-A, Lee JH, Baek N-I, Kim D-H. Antihyperlipidemic effect of Crocin isolated from the fructus of gardenia jasminoides and its metabolite crocetin. Biological and Pharmaceutical Bulletin. 2005;28(11):2106–10.doi:https://doi.org/10.1248/bpb.28.2106

55. Gupta S, Sharma SB, Bansal SK, Prabhu KM. Antihyperglycemic and hypolipidemic activity of aqueous extract of Cassia auriculata L. leaves in experimental diabetes. Journal of Ethnopharmacology. 2009;123(3):499–503.doi: https://doi.org/10.1016/j.jep.2009.02.019

56. Maniyar Y, Bhixavatimath P. Antihyperglycemic and hypolipidemic activities of aqueous extract of Carica papaya Linn. leaves in alloxan-induced diabetic rats. Journal of Ayurveda and Integrative Medicine. 2012;3(2):70.doi: 10.4103/0975-9476.96519

57. Assad T, Khan RA, Feroz Z. Evaluation of hypoglycemic and hypolipidemic activity of methanol extract of brassica oleracea. Chinese Journal of Natural Medicines. 2014;12(9):648–53.doi: 10.1016/s1875-5364(14)60099-6

58. Emordi JE, Agbaje EO, Oreagba IA, Iribhogbe OI. Antidiabetic and hypolipidemic activities of hydroethanolic root extract of uvaria chamae in streptozotocin induced diabetic albino rats. BMC Complementary and Alternative Medicine. 2016;16(1). doi: 10.1186/s12906-016-1450-0

59. Liu H, Qi X, Yu K, Lu A, Lin K, Zhu J, et al. AMPK activation is involved in hypoglycemic and hypolipidemic activities of mogroside-rich extract from siraitia grosvenorii (Swingle) fruits on high-fat diet/streptozotocin-induced diabetic mice. Food & Function. 2019;10(1):151–62.doi: 10.1039/C8FO01486H

60. Kim HY, Jeong DM, Jung HJ, Jung YJ, Yokozawa T, Choi JS. Hypolipidemic effects of Sophora flavescens and its constituents in poloxamer 407-induced hyperlipidemic and cholesterol-fed rats. Biological and Pharmaceutical Bulletin. 2008;31(1):73–8.doi:10.1248/bpb.31.73

61. Min S-W, Kim D-H. Kakkalide and Irisolidone: HMG-COA reductase inhibitors isolated from the flower of Pueraria Thunbergiana. Biological and Pharmaceutical Bulletin. 2007;30(10):1965–8.doi:https://doi.org/10.1248/bpb.30.1965

62. Ji W, Gong BQ. Hypolipidemic effects and mechanisms of Panax Notoginseng on lipid profile in hyperlipidemic rats. Journal of Ethnopharmacology. 2007;113(2):318–24. doi:https://doi.org/10.1016/j.jep.2007.06.022

63. Kwon S-H, Ahn I-S, Kim S-O, Kong C-S, Chung H-Y, Do M-S, et al. Anti-obesity and hypolipidemic effects of black soybean anthocyanins. Journal of Medicinal Food. 2007;10(3):552–6.doi:https://doi.org/10.1089/jmf.2006.147

64. Ko J-H, Lee S-J, Lim K-T. Hypolipidemic effect and antioxidant activity of glycoprotein isolated from Ulmus Davidiana Nakai in Triton WR-1339-treated mouse. Cell Biochemistry and Function. 2007;25(5):495–500.doi:https://doi.org/10.1002/cbf.1337

65. Lee C-L, Hung H-K, Wang J-J, Pan T-M. Red Mold Dioscorea has greater hypolipidemic and antiatherosclerotic effect than traditional red mold rice and unfermented Dioscorea in Hamsters. Journal of Agricultural and Food Chemistry. 2007;55(17):7162–9.doi:https://doi.org/10.1021/jf071293j

66. Trinh HT, Han SJ, Kim SW, Lee YC, Kim DH.Bifidus Fermentation Increases Hypolipidemic and Hypoglycemic Effects of Red Ginseng.Journal of Microbiology and Biotechnology.2007;17(7):1127-33.

67. Xie W, Wang W, Su H, Xing D, Cai G, Du L. Hypolipidemic mechanisms of ananas comosus L. leaves in mice: Different from fibrates but similar to statins. Journal of Pharmacological Sciences. 2007;103(3):267–74.doi: 10.1254/jphs.fp0061244

68. Chenni A, Yahia DA, Boukortt FO, Prost J, Lacaille-Dubois MA, Bouchenak M. Effect of aqueous extract of Ajuga Iva Supplementation on plasma lipid profile and tissue antioxidant status in rats fed a high-cholesterol diet. Journal of Ethnopharmacology. 2007;109(2):207–13.doi: https://doi.org/10.1016/j.jep.2006.05.036

69. Muthu AK, Sethupathy S, Manavalan R, Karar PK. Antioxidant potential of methanolic extract of dolichos biflorus Linn in high fat diet fed rabbits. Indian Journal of Pharmacology. 2006;38(2):131.doi:10.4103/0253-7613.24620

Received on 23.01.2023 Modified on 07.04.2023

Res. J. Pharmacology and Pharmacodynamics.2023;15(3):127-132.

DOI: 10.52711/2321-5836.2023.00023

Sr. No.	Hyperlipoproteinemia	Synonym	Occurrence	Defect	Enhanced lipoprotein
1	Type I	Primary hyperlipoproteinaemia or Familial hyperchylomicronemia	Very rare	Decreased lipoprotein lipase (LPL)	Chylomicrons
2	Type IIa	Polygenic hypercholesterolaemia or Familial hypercholesterolemia	Less common	LDL receptor deficiency	LDL
3	Type IIb	Combined hyperlipidemia	Commonest	Decreased LDL receptor and Increased ApoB	LDL and VLDL
4	Type III	Familial dysbetalipoproteinemia	Rare	Defect in Apo E 2 synthesis	IDL
5	Type IV	Familial hyperlipidemia	Common	Increased VLDL production and Decreased elimination	VLDL
6	Type V	Endogenous hypertriglyceridemia	Less common	Increased VLDL production and Decreased LPL	VLDL and Chylomicrons