https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1053/jhep.2003.50193

Nonalcoholic steatohepatitis: Summary of an AASLD Single Topic Conference

AGA technical review on nonalcoholic fatty liver disease

https://www.cell.com/trends/biochemical-sciences/pdf/S0968-0004(06)00332-X.pdf

Molecular biology of PCSK9: its role in LDL metabolism

https://www.journal-of-hepatology.eu/article/S0168-8278(13)00136-0/pdf

Cholesteryl ester storage disease: Review of the findings in 135 reported patients with an underdiagnosed disease

Nonalcoholic fatty liver disease (NAFLD) is an increasingly recognized cause of liver-related morbidity and mortality. It can develop secondary to numerous causes but a great majority of NAFLD cases occur in patients who are obese or present with other components of metabolic syndrome (hypertension, dyslipidemia, diabetes). This is called primary NAFLD and insulin resistance plays a key role in its pathogenesis. Obesity is characterized by expanded adipose tissue, which is under a state of chronic inflammation. This disturbs the normal storage and endocrine functions of adipose tissue. In obesity, the secretome (adipokines, cytokines, free fatty acids and other lipid moieties) of fatty tissue is amplified, which through its autocrine, paracrine actions in fat tissue and systemic effects especially in the liver leads to an altered metabolic state with insulin resistance (IR). IR leads to hyperglycemia and reactive hyperinsulinemia, which stimulates lipid-accumulating processes and impairs hepatic lipid metabolism. IR enhances free fatty acid delivery to liver from the adipose tissue storage due to uninhibited lipolysis. These changes result in hepatic abnormal fat accumulation, which may initiate the hepatic IR and further aggravate the altered metabolic state of whole body. Hepatic steatosis can also be explained by the fact that there is enhanced dietary fat delivery and physical inactivity. IR and NAFLD are also seen in various lipodystrophic states in contrary to popular belief that these problems only occur due to excessive adiposity in obesity. Hence, altered physiology of adipose tissue is central to development of IR, metabolic syndrome and NAFLD.

/pdf/metabolic-liver-disease-of-obesity-and-role-of-adipose-13hmagn8m5.pdf

Metabolic liver disease of obesity and role of adipose tissue in the pathogenesis of nonalcoholic fatty liver disease.

Liver Ultrastructure in Abetalipoproteinemia: Evolution of Micronodular Cirrhosis

Small intestinal mucosa in cholesterol ester storage disease. A light and electron microscope study.

Fatty liver in reyes syndrome is it a distinct morphologic entity

Bile acid malabsorption (BAM) following ileal resection (IR) may cause watery (cholerheic) diarrhea and/or steatorrhea(S). BAM was evaluated in 15 such patients: a)short bowel syndrome after IR; b)idiopathic intractable diarrhea(ID)(prolonged, severe diarrhea from birth of unknown etiology) requiring hyperalimentation to maintain life; c)miscellaneous steatorrhea(MS) (isolated pancreatic insufficiency or hypobetalipoproteinemia) and d) chronic nonspecific diarrhea(CD) without S. Following an oral test meal containing 10 jμCi14C cholic acid(14C) and a nonabsorbable marker PEG stools were collected for calculation of a 14C:PEG excretion ratio. In 9 patients (MS+CD) with moderate diarrhea the mean loss of 14C (6%) and excretion ratio (.07) are in marked contrast to IR and ID patients. There was no difference between IR and ID groups. Ileal function (Schilling test + IF) was grossly abnormal (<1%) in 2 IR and both ID patients. The cause of BAM in ID may be due to diffuse ileal disease or to a specific bile acid transport defect. (Support: NIH GCRC RR-123)

/pdf/bile-acid-malabsorption-in-infantile-diarrhea-3vpksej0y3.pdf

Bile acid malabsorption in infantile diarrhea

Electron microscopical (EM) and lipid histochemical studies have been made of liver biopsies from 3 abetalipoproteinemic (AB-LP) and 2 hypobetalipoproteinemic (HypoB-LP) children All AB-LP livers were enlarged and grossly fatty (38% lipid, 91% triglyceride [TG] ) By EM, endogenous tri-glyceride particles were absent Trans-Golgi vesicles and circum-Golgi smooth endoplasmic reticulum were absent Most lipid vacuoles were non-membrane-bounded This Golgi lesion has not been seen in other childhood fatty livers One AB-LP infant was biopsied at 10, 12, 24, 30 and 38 months, before, during and after treatment with a low-fat MCT diet During the interval of observation, he had persistent elevation of transaminases and he developed severe micronodular cirrhosis Alcoholic hyalin (AH) appeared in hepatocytes after MCT treatment; mitochondrial dense bodies increased in size and density Eight months after MCT was stopped, AH was greatly reduced and mitochondrial dense bodies normalized It is speculated the alcoholic hyalin was related to accumulation of acetate from MCT-fatty acids in the face of defective TG secretion in a manner biochemically analogous to hepatic ethanol metabolism MCT should be used cautiously in AB-LP infants until more data is available Support: NIH #RR-123

/pdf/micronodular-cirrhosis-in-abetalipoproteinemia-possible-4s7mbceb9p.pdf

Micronodular cirrhosis in abetalipoproteinemia: possible exacerbation by medium chain triglyceride (mct) feeding

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