Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats

Li, Shujun; Nussbaum, Michael S.; Teague, D. Maxwell; Gapen, Cynthia L.; Dayal, Rameshwar; Fischer, Josef E.

doi:10.1016/0022-4804(88)90095-9

Cited by 55 publications

(23 citation statements)

References 9 publications

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“…The etiology of this liver dysfunction is unknown. The liver injury has been hypothesized to be secondary to a lack of or excessive lipid calories, essential fatty acid deficiency, excessive dextrose, caloric excess, amino acid imbalance, and toxic manifestations of amino acids [21,22]. The increased incidence of cholestasis and subsequent hepatic failure has been associated with lack of enteral stimulation/feeding, recurrent sepsis, and intestinal bacterial overgrowth [23].…”

Section: Discussionmentioning

confidence: 99%

Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Thatch¹,

Schwartz²,

Yoo³

et al. 2008

Journal of Pediatric Surgery

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Section: Discussionmentioning

confidence: 99%

Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Thatch¹,

Schwartz²,

Yoo³

et al. 2008

Journal of Pediatric Surgery

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“…Potential etiologies related to hyperalimentation include the lack of or excessive lipid caloric intake by patient weight, essential fatty acid (FA) and amino acid deficiency, nutrient deficiency, excessive total caloric intake by patient weight, and amino acid imbalance and toxicity [9,22,23]. Lack of enteral stimulation and feeding, recurrent sepsis, and intestinal bacterial overgrowth are believed to be key exacerbating factors to this liver dysfunction [24].…”

Section: Discussionmentioning

confidence: 99%

Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Thatch

Katz

Haber

et al. 2010

Journal of Pediatric Surgery

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“…Some factors that induce the appearance of cholestasis are patient-specific: age, prolonged fasting, short bowel syndrome, septic episodes from intestinal bacterial translocation, surgery, etc., [1][2][3]. But there are also other factors directly linked to the route used and/or the composition of the nutrient mix, causing steatosis, cholangitis, and cholestasis [4][5][6][7][8][9][10]. Several studies have implicated diets with amino acid imbalances as the cause of TPN-AC [11,12].…”

Section: Introductionmentioning

confidence: 99%

Taurine and cholestasis associated to TPN. Experimental study in rabbit model

et al. 2005

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Taurine seems to be essential in the newborn for bile acid (BA) tauroconjugation, and its deficiency has been implicated in total parenteral nutrition-associated cholestasis (TPN-AC). Our purpose was to study the relationship between taurine (Ta) and TPN-AC in rabbits, which have a similar biliary metabolism to that of humans. We used 40 young rabbits, fed for 10 days according to the following four groups: GA [10] given TPN, with amino acid solution (AA) but without taurine (Ta) or its AA-precursors (methionine, cysteine, and serine); GB [10] the same but only without taurine; GC [10] the same but with taurine and its precursors; and GD [10] the control group with oral nutrition and saline infusion. Complete blood and bile analytical data were obtained and analyzed, including plasma AA and BA. Liver samples were studied under optical and electron microscopy. Serum: In GC there was a 20% increase in the AA-precursors, but paradoxically it was greater in GA. Bile: In GC there was 30% more excretion of total and free BA compared with less than 20% in GA and GB. Regarding toxic BA, there was a 15% decline in GLC3S excretion, but more than 20% in LCA excretion, than in GA and GB. Moreover, in GC the glyco-/tauro-conjugate ratio was worse than in the other groups. Histomorphology: While in GA and GB liver steatosis was diffuse (microsteatohepatitis type), in GC there was macrosteatosis with mitochondria-surrounded lipid droplets. In GA and GB, the canaliculi appeared dilated, with abundant bile plugs and loss of microvilli. There are signs that taurine may protect against TPN-AC. The mechanism does not seem to be BA tauroconjugation, but probably taurine's antioxidant, membrane stabilization (with Ca2+ and HCO3-), and/or osmotic effects.

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Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats

Cited by 55 publications

References 9 publications

Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Modulation of the inflammatory response and apoptosis using epidermal growth factor and hepatocyte growth factor in a liver injury model: a potential approach to the management and treatment of cholestatic liver disease

Growth factor modulation of hepatic inflammation: a novel approach to the management of total parenteral nutrition–associated liver disease

Taurine and cholestasis associated to TPN. Experimental study in rabbit model

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