Addition of l-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats

Li, Shujun; Nussbaum, Michael S.; McFadden, David W.; Zhang, Fusheng; LaFrance, R; Dayal, Rameshwar; Fischer, Josef E.

doi:10.1016/0022-4804(90)90006-n

Cited by 53 publications

(8 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In a rodent PN model, depletion of plasma glutamine was associated with the development of hepatic steatosis, and glutamine supplementation resulted in decreased steatosis 50, 51. However, rodent glutamine requirements are quite different from those of humans; in fact, glutamine supplementation for long‐term PN patients resulted in hepatic abnormalities in one study 52.…”

Section: Pathophysiologymentioning

confidence: 99%

Parenteral nutrition-associated liver disease and the role for isolated intestine and intestine/liver transplantation

2005

View full text Add to dashboard Cite

Parenteral nutrition-associated liver disease (PNALD) is the most devastating complication of long-term parenteral nutrition therapy. Because its progression is typically insidious and its long-term consequences are generally underappreciated, PNALD is often recognized too late, when liver injury is irreversible. When end-stage liver disease (ESLD) develops in these patients, most potential interventions are futile and transplantation of both an intestine and a liver becomes the only viable option, despite the relatively poor outcomes associated with this combined procedure. Although likely multifactorial in origin, the etiology of PNALD is poorly understood. Early clinical intervention with a combination of nutritional, medical, hormonal, and surgical therapies can be effective in preventing liver disease progression. If these interventions fail, intestinal transplantation should be performed expeditiously before development of ESLD mandates simultaneous inclusion of a liver graft as well. (HEPATOLOGY 2006;43:9-19.)

show abstract

Section: Pathophysiologymentioning

confidence: 99%

Parenteral nutrition-associated liver disease and the role for isolated intestine and intestine/liver transplantation

2005

View full text Add to dashboard Cite

show abstract

“…Therefore, raising the insulin-to-glucagon ratio disturbs fat metabolism and causes the deposition of fat in liver and other tissue, whereas lowering the ratio has the opposite effect. [9][10][11] In the present study, the addition of lipid to the TPN solution (even in excess of caloric needs) had no effect upon portal glucagon levels, although it lowered the portal insulin levels and prevented hepatic steatosis.…”

Section: Discussionmentioning

confidence: 75%

Addition of Lipid to Total Parenteral Nutrition Prevents Hepatic Steatosis in Rats by Lowering the Portal Venous Insulin/Glucagon Ratio

Nussbaum

Bower

et al. 1992

J Parenter Enteral Nutr

Self Cite

View full text Add to dashboard Cite

Hepatic steatosis in rats is associated with an infusion of excessive carbohydrate calories. Previous work from this laboratory suggested that this is associated with an elevated portal insulin/glucagon molar ratio (I/G) and is reversed by parenteral glucagon administration. Although hepatic steatosis is not related to essential fatty acid deficiency, addition of lipid to total parenteral nutrition (TPN) has been reported as being protective against the development of hepatic steatosis. Therefore, we propose that lipid may exert its salutary effect via an alteration of the I/G ratio. To test this hypothesis, adult rats (seven per group) received internal jugular catheters: group 1, saline (3 mL/h) plus chow ad libitum; group 2, 25% dextrose base TPN; group 3, 17% dextrose base TPN + 2.5% lipid; group 4, 25% dextrose base TPN + 2.5% lipid. At 7 days, portal and peripheral venous blood was drawn for insulin and glucagon radioimmunoassay and liver function tests; livers were removed for histology and lipid content determination. Panlobular vacuolization, on histology, and lipid content were excessive in group 2, and the portal I/G was increased because of elevated portal insulin. In contrast, portal venous insulin and I/G did not increase, and hepatic steatosis was absent in groups 3 and 4. The results suggest that the addition of lipid to TPN in rats decreases the portal insulin level and lowers the portal I/G, and thereby prevents hepatic steatosis.

show abstract

“…In a study of adult rats, portal glucagon concentrations were found to be significantly elevated in glutamine-supplemented rats compared with controls. 108 Furthermore, hepatic lipid content did not increase in this supplemented group. Preliminary human studies are clearly needed to confirm the relevance of these findings from animal models.…”

Section: Tpnmentioning

confidence: 74%

“…5,95,96,[103][104][105] Numerous studies indicate that increasing the dextrose concentration correlates with increasing hepatic lipid accumulation. The work of Li et al [106][107][108] has also shown that this increase in dextrose concentration results in elevated portal insulin/glucagon ratios in rat models. A follow-up study with the addition of glucagon to the TPN formula prevented hepatic lipid accumulation.…”

Section: Tpnmentioning

confidence: 99%

Metabolic and nutritional considerations in nonalcoholic fatty liver

et al. 2000

View full text Add to dashboard Cite

Addition of l-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats

Cited by 53 publications

References 13 publications

Parenteral nutrition-associated liver disease and the role for isolated intestine and intestine/liver transplantation

Parenteral nutrition-associated liver disease and the role for isolated intestine and intestine/liver transplantation

Addition of Lipid to Total Parenteral Nutrition Prevents Hepatic Steatosis in Rats by Lowering the Portal Venous Insulin/Glucagon Ratio

Metabolic and nutritional considerations in nonalcoholic fatty liver

Contact Info

Product

Resources

About