Production of chylomicron-like lipoproteins from endogenous lipid by the intestine and liver of diabetic dogs

Steiner, George; Poapst, M.; Davidson, J. K.

doi:10.2337/diabetes.24.3.263

Cited by 27 publications

(16 citation statements)

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“…Moreover, the transport of newly synthesized cholesterol from the small intestine to the circulation is increased fourfold in diabetic animals (40). Furthermore, several investigators have shown that the transport oftriglyceride from the small intestine to the circulation in the postabsorptive state is also increased by diabetes (41)(42)(43). These studies indicate that the flux of lipid from the small intestine to the circulation is enhanced by diabetes, and it is possible that the increase in oxidized lipid transport is related to these alterations in the lipid flux.…”

Section: Discussionmentioning

confidence: 71%

The effect of oxidized lipids in the diet on serum lipoprotein peroxides in control and diabetic rats.

Staprãns¹,

Rapp²,

Pan³

et al. 1993

J. Clin. Invest.

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The levels of oxidized serum lipoproteins are increased in humans and animals with diabetes. We have examined the contribution of dietary oxidized lipids on the levels of oxidized lipoproteins. In both control and streptozocin induced diabetic rats, the oxidized lipid content of mesenteric lymph chylomicrons (CM) increased when increasing quantities of oxidized lipids were administered intragastrically. However, at all levels of administered oxidized lipids, the quantity of oxidized lipids in CM was greater in the diabetic animals. These results indicate that oxidized lipids are absorbed and packaged into CM and suggest that there is increased absorption of oxidized lipids in diabetic animals. In nondiabetic rats fed a fat-free diet, the levels of oxidized lipids in their serum lipoproteins were very low. When oxidized lipids were added to the diet, the quantity of peroxides in serum lipoproteins increased about fivefold. In diabetic animals fed a fat-free diet, there were also very low levels of oxidized lipids in their serum lipoproteins, and there was no difference between control and diabetic rats. However, when diabetic animals were fed a diet containing oxidized lipids, the quantity of oxidized lipids in their serum lipoproteins increased 16-fold and were significantly greater than in controls. Thus, in both control and diabetic rats the quantity of oxidized lipids in the diet largely determines the levels of oxidized lipids in circulating lipoproteins. However, in diabetic animals the effect of diet is more pronounced. Together with the CM studies, these results demonstrate that dietary oxidized lipids make a major contribution to the levels of oxidized lipids in circulating lipoproteins and indicate that increased absorption of oxidized lipids in diabetic animals may play a role in the elevation of oxidized lipoproteins observed in this disorder. (J.

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Section: Discussionmentioning

confidence: 71%

The effect of oxidized lipids in the diet on serum lipoprotein peroxides in control and diabetic rats.

Staprãns¹,

Rapp²,

Pan³

et al. 1993

J. Clin. Invest.

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“…25) earlier studies indicate that increased TG absorption from intestine contributes to hypertriglyceridemia in diabetes. 26) Serum TG concentration was high and was decreased by the treatment of pioglitazone in ddY-H mice, but not in ddY-L mice. This finding suggest, in ddY-H mice, clearance of TG from circulation may function but may decrease to some extent, since lipoprotein lipase is activated by pioglitazone, an clearance of serum lipid was increased.…”

Section: Discussionmentioning

confidence: 92%

Hepatic Steatosis with Relation to Increased Expression of Peroxisome Proliferator-Activated Receptor-γ in Insulin Resistant Mice

Satoh

Ide

Kagawa

et al. 2013

Biological & Pharmaceutical Bulletin

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We have isolated insulin resistant mice (ddY-H mice) which are spontaneously induced even if fed with the standard chow pellets. Since marked accumulation of triglycerides (TG) in liver was observed, the present study investigated causes of hepatic TG accumulation in ddY-H mice fed with the standard chow pellets. In ddY-H mice, hepatic TG content increased from seven-weeks of age, and further marked accumulation of TG was observed at 20-weeks of age. Histologically, fat droplets appeared in pericentral parenchymal cells of the liver from nine-weeks of age, and the size and number of droplets were increased in hepatic lobules at 15-weeks of age, suggesting hepatic steatosis was spontaneously induced. Although secretion of TG from liver to blood in ddY-H mice was not increased, fat absorption from the digestive tract was significantly enhanced. The mRNA expressions of peroxisome proliferator-activated receptor γ (PPARγ) involved in fat accumulation and fatty acid translocase (CD36) involved in the transportation of fatty acid into the liver were markedly increased. However, gene expressions of factors involved in lipogenesis, β-oxidation of fatty acid and lipoprotein secretion were not changed. Pioglitazone (9 mg/kg), the PPARγ agonist, administered for six weeks deteriorated hepatic steatosis in ddY-H mice. Although pioglitazone did not affect gene expressions of PPARγ in the liver, CD36 and fat-specific protein 27 (fsp27), targets of PPARγ, were markedly elevated. These results suggest that, in the livers of ddY-H mice, hepatic steatosis is induced by increased incorporation of fatty acid into the liver via increased PPARγ expression.

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“…Tracer studies in pancreatectomized dogs suggested that circulating FFA might enter the intestinal mucosal cells directly and be esterified and secreted in intestinal lipoproteins. 30 We have recently demonstrated that acute elevation of plasma FFA by Intralipid/heparin (IH) infusion in chow-fed hamster increased intestinal apoB-48 production rate. 31 Furthermore, oleic acid perfusion of primary hamster enterocytes has been shown to increase the number of secreted apoB-48 -containing lipoprotein particles.…”

mentioning

confidence: 99%

Both Intestinal and Hepatic Lipoprotein Production Are Stimulated by an Acute Elevation of Plasma Free Fatty Acids in Humans

et al. 2008

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Background-Hepatic lipoprotein production has been shown previously to be regulated by free fatty acid (FFA) flux to the liver, whereas intestinal lipoprotein production is stimulated mainly by ingested fat absorbed from the intestinal lumen. Emerging evidence indicates that intestinal lipoprotein production is increased in insulin resistance and type 2 diabetes mellitus, conditions that are associated with increased levels of circulating FFAs. Here we investigated whether short-term elevation of plasma FFAs stimulates intestinal apolipoprotein (apo) B-48 -and hepatic apoB-100 -containing triglyceride-rich lipoprotein (TRL) production in humans in the fed state. Methods and Results-TRL apoB-48 and apoB-100 metabolism were examined in 12 healthy men during a constant fed state. The studies were as follows, respectively: (1) Intralipid/heparin was infused intravenously immediately before and during the kinetics study to induce an Ϸ3-fold difference in plasma FFA compared with the saline study; (2) saline was infused intravenously as a control. ApoB-48 -and apoB-100 -containing TRL production and clearance were determined with a 12-hour primed constant infusion of [D3]L-leucine and multicompartmental kinetic modeling. TRL apoB-48 production rate was 69% higher in the Intralipid/heparin study than in the saline control (5.95Ϯ1.13 versus 3.53Ϯ0.58 mg/kg per day; Pϭ0.027), and there was no significant difference in TRL apoB-48 clearance. TRL apoB-100 concentrations were also increased (PϽ0.001) and TRL apoB-100 production rate was 35% higher in the Intralipid/ heparin study compared with saline (28Ϯ4 versus 21Ϯ3 mg/kg per day; Pϭ0.020). Conclusions-This is the first study to demonstrate that intestinal TRL apoB-48 production is increased after short-term elevation of plasma FFAs in humans in the fed state, similar to the well-described stimulation of hepatic TRL apoB100 -containing particles by FFAs.

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Production of chylomicron-like lipoproteins from endogenous lipid by the intestine and liver of diabetic dogs

Cited by 27 publications

References 0 publications

The effect of oxidized lipids in the diet on serum lipoprotein peroxides in control and diabetic rats.

The effect of oxidized lipids in the diet on serum lipoprotein peroxides in control and diabetic rats.

Hepatic Steatosis with Relation to Increased Expression of Peroxisome Proliferator-Activated Receptor-γ in Insulin Resistant Mice

Both Intestinal and Hepatic Lipoprotein Production Are Stimulated by an Acute Elevation of Plasma Free Fatty Acids in Humans

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