Severe steatosis resulted from anorexia nervosa leading to fatal hepatic failure

Sakada, Michinori; Tanaka, Atsushi; Ohta, Daisuke; Takayanagi, Motoe; Kodama, Takeko; Suzuki, Koyu; Inoue, Kazuaki; Fujita, Yoshiyuki; Maruyama, Masataka

doi:10.1007/s00535-006-1845-7

Cited by 53 publications

(61 citation statements)

References 6 publications

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“…In that case, continuous infusion of 400 kcal a day had been prescribed but the patient discarded the contents of the infusion bag, and it could not be the case in the present subject. Another case of hepatic steatosis and fatal hepatic failure after total parenteral nutrition was reported, in which a hypoglycemic episode was observed (15). What was different from the present case was that total parenteral nutrition but not oral ingestion induced or worsened fatty liver changes that resulted in hepatic failure.…”

Section: Discussioncontrasting

confidence: 52%

Hypoglycemic Coma in a Patient with Anorexia Nervosa Coincident with Acute Exacerbation of Liver Injury Induced by Oral Intake of Nutrients

et al. 2010

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A 33-year-old woman with anorexia nervosa was admitted because of severe malnutrition. Acute liver injury was observed soon after the beginning of oral intake. She was prohibited from eating for 10 days and treated with parenteral nutrition until liver dysfunction was improved. One week after resuming oral intake, she presented severe hypoglycemic coma along with acute exacerbation of hepatocytic injury. Clinical laboratory data suggest that insufficient gluconeogenesis in acute liver injury was involved in severe hypoglycemia. We should be careful of severe hypoglycemia in patients with anorexia nervosa after resuming oral ingestion when signs of liver damage are detected, although hypoglycemic coma is uncommon in anorexia nervosa.

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Section: Discussioncontrasting

confidence: 52%

Hypoglycemic Coma in a Patient with Anorexia Nervosa Coincident with Acute Exacerbation of Liver Injury Induced by Oral Intake of Nutrients

et al. 2010

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“…This has been attributed to the unique metabolic capacity of the liver that esterifies exogenous fatty acids into TG and secretes VLDL (26). Indeed, fatty liver is seen commonly in starvation and anorexia nervosa when the lipolysis of adipose tissue increases circulating lipids (39,49). Interestingly, we observed that ADFP protein levels in islets are elevated during fasting when the energy status does not favor lipid storage.…”

Section: E253 Role Of Adipophilin In Lipid Metabolism In Islets 57)supporting

confidence: 54%

Adipose differentiation-related protein regulates lipids and insulin in pancreatic islets

Faleck

Ali

Roat

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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The excess accumulation of lipids in islets is thought to contribute to the development of diabetes in obesity by impairing ␤-cell function. However, lipids also serve a nutrient function in islets, and fatty acids acutely increase insulin secretion. A better understanding of lipid metabolism in islets will shed light on complex effects of lipids on ␤-cells. Adipose differentiation-related protein (ADFP) is localized on the surface of lipid droplets in a wide range of cells and plays an important role in intracellular lipid metabolism. We found that ADFP was highly expressed in murine ␤-cells. Moreover, islet ADFP was increased in mice on a high-fat diet (3.5-fold of control) and after fasting (2.5-fold of control), revealing dynamic changes in ADFP in response to metabolic cues. ADFP expression was also increased by addition of fatty acids in human islets. The downregulation of ADFP in MIN6 cells by antisense oligonucleotide (ASO) suppressed the accumulation of triglycerides upon fatty acid loading (56% of control) along with a reduction in the mRNA levels of lipogenic genes such as diacylglycerol O-acyltransferase-2 and fatty acid synthase. Fatty acid uptake, oxidation, and lipolysis were also reduced by downregulation of ADFP. Moreover, the reduction of ADFP impaired the ability of palmitate to increase insulin secretion. These findings demonstrate that ADFP is important in regulation of lipid metabolism and insulin secretion in ␤-cells. MIN6 cells; oleic acid; palmitic acid; high-fat diet; fasting THE CURRENT EPIDEMIC OF OBESITY is feared to increase the prevalence of type 2 diabetes due to its contribution to insulin resistance (38). However, excess adiposity and dyslipidemia commonly seen in obesity may have an additional role in the development of diabetes by directly damaging ␤-cells (45). Indeed, prolonged exposure to elevated levels of fatty acids impairs insulin secretion in vivo and ex vivo, a phenomenon termed "lipotoxicity" (16,47,50,56). Ceramide generation, an increase in reactive oxygen species, 12/15-lipoxygenase activation, and atypical protein kinase C activation are some of the mechanisms proposed for islet dysfunction and lipid-induced apoptosis (5, 44, 51, 52). On the other hand, lipids serve a nutrient function and are the principal energy source in islets deprived of exogenous nutrients (34, 54). Not only does acute exposure to fatty acids augment insulin secretion ex vivo, but a rise in fatty acids also facilitates glucose-stimulated insulin secretion (GSIS) after fasting in vivo (10). The activation of cell surface fatty acid receptor G protein-coupled receptor 40 (GPR40) plays a significant role in the augmentation of insulin secretion by fatty acids. However, cellular uptake of fatty acids is also believed to contribute to the insulin secretion by provision of lipid metabolites, including long-chain acyl-CoA and diacylglycerides (25,43,65). Thus, fatty acids play complex and seemingly contradictory roles in ␤-cells, which calls for a better understanding of fatty acid uptake, storage...

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“…In contrast, steatosis can also be produced by food deprivation, because fat is mobilized from adipose tissue to liver for acetyl-CoA production. Steatosis has been observed with anorexia (Sakada et al, 2006). Few studies have addressed how steatosis can affect Ugt expression and activity and whether excess fat stores can counter fasting-mediated alterations in enzyme expression or activity.…”

Section: Introductionmentioning

confidence: 99%

UDP-Glucuronosyltransferase Expression in Mouse Liver Is Increased in Obesity- and Fasting-Induced Steatosis

Xu¹,

Kulkarni²,

Li³

et al. 2011

Drug Metab Dispos

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ABSTRACT:UDP-glucuronosyltransferases (Ugt) catalyze phase II conjugation reactions with glucuronic acid, which enhances chemical polarity and the elimination from the body. Few studies have addressed whether Ugt expression and activity are affected by liver disease, such as steatosis. The purpose of this study was to determine whether steatosis induced by obesity or fasting could affect liver Ugt mRNA expression and activity. Male C57BL/6J and Lep ob/ob (ob/ob) mice were fed ad libitum or food was withheld for 24 h. In steatotic livers of ob/ob mice, Ugt1a1, -1a6, -1a9, -2a3, -3a1, and -3a2 mRNA expression increased. Fasting, which also induced steatosis, increased hepatic Ugt1a1, -1a6, -1a7, -1a9, -2b1, -2b5, -2a3, -3a1, and -3a2 mRNA expression in mouse liver. Likewise, acetaminophen glucuronidation increased by 47% in hepatic microsomes from ob/ob mice compared with that in C57BL/6J mice, but not after fasting. In both steatosis models, Ugt induction was accompanied by increased aryl hydrocarbon receptor, constitutive androstane receptor (CAR), peroxisome proliferator-activated receptor (PPAR)-␣, pregnane X receptor, nuclear factor (erythroidderived 2)-like 2 (Nrf2), and peroxisome proliferator-activated receptor-␥ coactivator-1␣ mRNA expression. In addition, fasting increased CAR, PPAR, and Nrf2 binding activity. The work points to hepatic triglyceride concentrations corresponding with nuclear receptor and Ugt expression. The findings indicate that steatosis significantly alters hepatic Ugt expression and activity, which could have a significant impact on determining circulating hormone levels, drug efficacy, and environmental chemical clearance.

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Severe steatosis resulted from anorexia nervosa leading to fatal hepatic failure

Cited by 53 publications

References 6 publications

Hypoglycemic Coma in a Patient with Anorexia Nervosa Coincident with Acute Exacerbation of Liver Injury Induced by Oral Intake of Nutrients

Hypoglycemic Coma in a Patient with Anorexia Nervosa Coincident with Acute Exacerbation of Liver Injury Induced by Oral Intake of Nutrients

Adipose differentiation-related protein regulates lipids and insulin in pancreatic islets

UDP-Glucuronosyltransferase Expression in Mouse Liver Is Increased in Obesity- and Fasting-Induced Steatosis

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