Effects of insulin on plasma lipoproteins in diabetic ketoacidosis: evidence for a change in high density lipoprotein composition during treatment. 1982

S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin

To determine the acute effects of insulin on lipoprotein metabolism, we have followed the plasma lipoprotein lipid and apolipoprotein levels during insulin therapy for the first 24 hr in 13 patients with diabetic ketoacidosis. Corrections were made for plasma volume changes during treatment. Before insulin treatment, mean plasma triglyceride and cholesterol levels were 574 mg/dl (range 53-2355) and 212 mg/dl (range 118-416), respectively. Insulin therapy resulted in rapid decreases in triglyceride-rich lipoproteins, chylomicrons, and very low density lipoproteins (VLDL), with most patients achieving plasma triglyceride levels below 150 mg/dl at 24 hr. Mean basal levels of intermediate density lipoproteins (IDL) and low density lipoproteins (LDL)-cholesterol were low (9.9 and 72 mg/dl, respectively) and were statistically invariant with therapy. Mean basal levels of high density lipoprotein (HDL) cholesterol were also low (26 mg/dl, range 5-48) and were invariant during the first 12 hr and increased significantly to 29 mg/dl by the 24th hr. Plasma apoprotein (apo) B levels were in the upper normal range (101 mg/dl) before treatment and decreased with therapy due to significant decreases in VLDL, but not IDL or LDL apoB. VLDL appeared to have a normal apoprotein composition which did not change with treatment. Mean apoA-I levels which were near normal in plasma and HDL before therapy, decreased significantly (16%) by 12 hr and subsequently increased towards basal levels between 12 and 24 hr. The ratio of apoA-I to cholesterol in HDL also fell significantly during the entire 24 hr. Density gradient ultracentrifugal analysis of the d > 1.006 g/ml fractions indicated a selective decrease in "lighter" density fractions of HDL-apoA-I during treatment. These results provide evidence that insulin may decrease the secretion of apoA-I into plasma or increase catabolism.-Weidman, S. W., J. B. Ragland, J. N. Fisher, Jr., A. E. Kitabchi, and S. M. Sabesin. Effects of insulin on plasma lipoproteins in diabetic ketoacidosis: evidence for a change in high density lipoprotein composition composition during treatment.

UI MeSH Term Description Entries
D007328 Insulin A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1). Iletin,Insulin A Chain,Insulin B Chain,Insulin, Regular,Novolin,Sodium Insulin,Soluble Insulin,Chain, Insulin B,Insulin, Sodium,Insulin, Soluble,Regular Insulin
D008075 Lipoproteins, HDL A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases. High Density Lipoprotein,High-Density Lipoprotein,High-Density Lipoproteins,alpha-Lipoprotein,alpha-Lipoproteins,Heavy Lipoproteins,alpha-1 Lipoprotein,Density Lipoprotein, High,HDL Lipoproteins,High Density Lipoproteins,Lipoprotein, High Density,Lipoprotein, High-Density,Lipoproteins, Heavy,Lipoproteins, High-Density,alpha Lipoprotein,alpha Lipoproteins
D008079 Lipoproteins, VLDL A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues. Pre-beta-Lipoprotein,Prebeta-Lipoprotein,Prebeta-Lipoproteins,Very Low Density Lipoprotein,Very-Low-Density Lipoprotein,Very-Low-Density Lipoproteins,Lipoprotein VLDL II,Lipoproteins, VLDL I,Lipoproteins, VLDL III,Lipoproteins, VLDL1,Lipoproteins, VLDL2,Lipoproteins, VLDL3,Pre-beta-Lipoproteins,Lipoprotein, Very-Low-Density,Lipoproteins, Very-Low-Density,Pre beta Lipoprotein,Pre beta Lipoproteins,Prebeta Lipoprotein,Prebeta Lipoproteins,VLDL Lipoproteins,VLDL1 Lipoproteins,VLDL2 Lipoproteins,VLDL3 Lipoproteins,Very Low Density Lipoproteins
D008297 Male Males
D008875 Middle Aged An adult aged 45 - 64 years. Middle Age
D005260 Female Females
D005500 Follow-Up Studies Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease. Followup Studies,Follow Up Studies,Follow-Up Study,Followup Study,Studies, Follow-Up,Studies, Followup,Study, Follow-Up,Study, Followup
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000293 Adolescent A person 13 to 18 years of age. Adolescence,Youth,Adolescents,Adolescents, Female,Adolescents, Male,Teenagers,Teens,Adolescent, Female,Adolescent, Male,Female Adolescent,Female Adolescents,Male Adolescent,Male Adolescents,Teen,Teenager,Youths
D000328 Adult A person having attained full growth or maturity. Adults are of 19 through 44 years of age. For a person between 19 and 24 years of age, YOUNG ADULT is available. Adults

Related Publications

S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
April 1985, Diabete & metabolisme,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
October 1987, Atherosclerosis,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
October 1985, Obstetrics and gynecology,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
July 1987, Clinical and investigative medicine. Medecine clinique et experimentale,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
October 1993, European journal of clinical investigation,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
February 1996, Diabetic medicine : a journal of the British Diabetic Association,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
June 1992, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
January 1974, Scandinavian journal of clinical and laboratory investigation. Supplementum,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
January 1981, Artery,
S W Weidman, and J B Ragland, and J N Fisher, and A E Kitabchi, and S M Sabesin
April 1983, Biochemical medicine,
Copied contents to your clipboard!