The Response of Plasma Triglyceride, Cholesterol, and Lipoprotein Lipase to Treatment in Non-insulin-dependent Diabetic Subjects Without Familial Hypertriglyceridemia

Pfeifer, Michael; Brunzell, John D.; Best, James D.; Judzewitsch, R.; Halter, Jeffrey B.; Porte, Daniel

doi:10.2337/diab.32.6.525

Cited by 69 publications

(38 citation statements)

References 7 publications

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“…Our results demonstrated a marked increase in adipose tissue LPL activity during insulin therapy. The improvement of glycemic control by sulfonylureas was also followed by a rise of adipose LPL activity 12 -^ **•** as well as by an increase in the fractional catabolic rates of both VLDL triglyceride and VLDL apo B. 39 This indicates that the elevation of LPL activity is of physiological significance and probably contributes to the fall of VLDL level.…”

Section: Insulin Therapy and Llpolytlc Enzymesmentioning

confidence: 90%

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Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.

et al. 1988

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To study the effects of rigorous insulin therapy on serum lipoproteins in patients with noninsulin-dependent diabetes not controlled with oral agents only, we measured serum lipoproteins, apoproteins, lipolytic enzymes, and glucose disposal using an insulin clamp technique before and after 4 weeks of insulin therapy. Lipoproteins were isolated by ultracentrifugation and high density lipoprotein (HDL) subfractions, by rate-zonal density gradient ultracentrifugation. The group included 11 women and eight men (age 58 +/- 1 years and RBW 125 +/- 4%). Body weight, glycosylated hemoglobin, mean diurnal glucose, plasma free insulin, and glucose uptake (M-value) were 75 vs. 76 kg; 11.9 vs. 8.9%; 234 vs. 124 mg/dl; 12 vs. 27 microU/ml; and 5.0 +/- 0.4 vs. 7.1 +/- 0.6 mg/kg/min before and after insulin therapy, respectively. After insulin therapy there was a decrease of very low density lipoprotein (VLDL) triglyceride (-60%, p less than 0.001) but an increase of HDL2 cholesterol (+21%, p less than 0.001); HDL2 phospholipids (+38%, p less than 0.001); HDL2 proteins (+23%, p less than 0.01); and HDL2 mass (127 +/- 11 vs. 158 +/- 12 mg/dl, p less than 0.001). There was a decrease of HDL3 cholesterol (-13%, p less than 0.05); HDL3 phospholipids (-16%, p less than 0.05); HDL3 proteins (-18%, p less than 0.001); and HDL3 mass (179 +/- 6 vs. 146 +/- 6, p less than 0.01). Zonal profiles showed a redistribution of particles from HDL3 to HDL2. Serum apo A-I increased (p less than 0.05), apo A-II remained constant, but apo B decreased (-29%, p less than 0.001). The most marked change during insulin therapy was a 2.3-fold increase in adipose tissue lipoprotein lipase (LPL) activity (p less than 0.001). The changes of VLDL and HDL subfractions were not explained by respective changes of the blood glucose, free insulin, or M-value. The data indicate that intensive insulin therapy induces antiatherogenic changes in serum lipids and lipoproteins and suggest that the induction of LPL by insulin is the major factor responsible for redistribution of HDL particles from HDL3 to HDL2.

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Section: Insulin Therapy and Llpolytlc Enzymesmentioning

confidence: 90%

“…12 -3 Plasma HDL levels are regulated by the two lipolytic enzymes; lipoprotein Iipase and hepatic Iipase activities, by the LCAT reaction, by the metabolism of apo A-l and A-ll, and by the lipid transfer processes. 15 ' 5S Hepatic Iipase is a phospholipase, which degrades HDL2 phospholipids.…”

Section: Insulin Therapy and High Density Llpoprotelnmentioning

confidence: 99%

Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.

et al. 1988

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“…The protein was measured by the method of Lowry using bovine serum albumin as a standard. Specific activity of the enzyme was expressed as pmol of [1][2][3][4][5][6][7][8][9][10][11][12][13][14] C]-palmitoyl-CoA formed per min per mg protein.…”

Section: Analysis Of Hepatic Lipidsmentioning

confidence: 99%

“…Triglycerides and apolipoprotein B 100 are assembled into very-low density lipoprotein (VLDL) with the aid of microsome triglyceride transfer protein (MTP) and secreted into the blood. Hypertriglyceridemia seen in diabetic subjects is mainly the result of a decrease in the activity of lipoprotein lipase, an insulin-activated enzyme responsible for clearance of plasma triglycerides [11,12] and/or an increased VLDL production in the liver [13,14].…”

Section: Introductionmentioning

confidence: 99%

Effect of pinealectomy on plasma levels of insulin and leptin and on hepatic lipids in type 2 diabetic rats

Nishida

Sato

Murai

et al. 2003

Journal of Pineal Research

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: We previously reported that pharmacological melatonin administration to type 2 diabetic rats reduces hyperinsulinemia and improves the altered fatty‐acid metabolism. To determine whether melatonin deficiency exacerbates diabetes‐associated conditions, we investigated the effect of pinealectomy (i.e. melatonin‐deficiency) on plasma hormone levels and lipid metabolism in type 2 diabetic Otsuka Long‐Evans Tokushima Fatty (OLETF) rats. We compared levels of insulin and leptin, and hepatic lipids in pinealectomized OLETF (PO) rats, sham‐operated OLETF (SO) rats and sham‐operated healthy Long‐Evans Tokushima Otsuka (LETO) (SL) rats 16 and 30 wk after the operation. Plasma glucose and triglycerides were increased in SO and PO rats 30 wk after operation compared with age‐matched SL rats. Pinealectomy caused an increase in free cholesterol among the plasma lipids, as compared with SO rats. Sixteen weeks after pinealectomy, typical hyperinsulinemia was observed in PO rats (3.47‐fold increase, P < 0.01) as compared with SL rats, whereas at 30 wk, the plasma levels of insulin in PO and SO rats had decreased and there was no significant difference among the three groups. Hepatic triglycerides were increased (1.54‐fold, P < 0.005) in PO rats, compared with SO rats. Hepatic acyl‐CoA synthetase (ACS) activity was significantly augmented in PO rats at 30 wk (10%, P < 0.01 versus SO group), while microsomal triglyceride transfer protein (MTP) decreased (−27% versus SO, P < 0.05); thus, the increased ACS activity and decreased MTP might have a role in the accumulation of hepatic triglycerides in PO rats. In summary, pinealectomy causes severe hyperinsulinemia and accumulation of triglycerides in the liver, probably owing to the loss of the nocturnal melatonin surge.

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“…Although, this has not been resolved completely, delayed clearance of TRL secondary to decreased LPL activity is believed to be the most important mechanism with some contribution from excessive 20,21 hepatic Tg production .…”

Section: Discussionmentioning

confidence: 99%

Postprandial Lipid Abnormalities in Type 2 Diabetes Mellitus, A Study at NGMC, Kohalpur

Shukla

2017

J. Nepalgunj Med. College

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Aim and Objectives:To study the postprandial lipid abnormalities in patients with type 2 diabetes mellitus. Material and Methods : Postprandial lipids were studied in 40 male type 2 diabetic subjects (age 49.75 ± 4.82 years) and 40 age and sex matched healthy controls (age 49.55 ± 4.82 years) after an oral fat challenge which consisted of a meal providing 729 kcal/m2 body surface area with 68 gm fat. Results: Average duration of diabetes among diabetic was 2.32 ± 3.03 years. The body mass index (cases 25.84 ± 4.52; controls 25.74 ± 5.0; p > 0.05) and waist-hip ratio (cases 1.06 ± 0.13; controls 1.14 ± 0.2; p > 0.05) were similar in both groups. While fasting serum lipids were not significantly different between the two groups, a number of serum lipid abnormalities were noted in type 2 diabetic subjects in the postprandial state. These included a higher triglyceride-area under curve (AUC) (cases 1298.08 ± 485.2 vs. controls 922.15 ± 390.47 mg/dl/8h; p=0.01), a higher triglyceride-area under incremental curve (AUIC) (cases 549.68 ± 382.24; control 294.75 ± 172.6 mg/dl/8h; p=0.01), a higher peak triglyceride level (cases 425.2 ± 204.47 mg%, controls 283.9 ± 11.6.94 mg%, p=0.01), a lower HDL-AUC (cases 130.35 ± 33.55 vs. controls 168.48 ± 56.01 mg/dl/8h, p=0.013) and a lower HDL nadir (Cases 28.05 ± 10.94 mg%, controls 37.13 ± 13.52 mg%, p < 0.02). Triglyceride AUC correlated significantly with fasting serum triglyceride (r=0.62) and BMI (r=0.7), but not with waist hip ratio . Postprandial lipaemia did not correlate with age, duration of diabetes, fasting blood glucose or glycosylated hemoglobin. Conclusion: In conclusion, type 2 diabetics demonstrate significant postprandial lipid abnormalities, particularly of triglycerides, which appear to be independent of glycaemic control.

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The Response of Plasma Triglyceride, Cholesterol, and Lipoprotein Lipase to Treatment in Non-insulin-dependent Diabetic Subjects Without Familial Hypertriglyceridemia

Cited by 69 publications

References 7 publications

Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.

Insulin therapy induces antiatherogenic changes of serum lipoproteins in noninsulin-dependent diabetes.

Effect of pinealectomy on plasma levels of insulin and leptin and on hepatic lipids in type 2 diabetic rats

Postprandial Lipid Abnormalities in Type 2 Diabetes Mellitus, A Study at NGMC, Kohalpur

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