Fatty liver deposition and sparing: a pictorial review.

OBJECTIVE: Fatty liver deposition is a very common finding, but it has many atypical patterns of distribution that can represent diagnostic pitfalls. The purpose of this pictorial essay is to review different patterns of fatty liver deposition and sparing. METHODS: We searched our archive retrospectively, reviewed the literature, and identified six patterns of liver steatosis. RESULTS: Steatosis may be diffuse, geographic, focal, subcapsular, multifocal or perivascular. CONCLUSIONS: Previous knowledge of atypical patterns of steatosis distribution may prevent misdiagnosis of infiltrative disease or focal liver lesions. When an unusual form of fatty liver deposition is suspected on ultrasound or computed tomography, magnetic resonance imaging may be used to confirm the diagnosis.

The Sp transcription factors are involved in the cellular expression of the human glucose-dependent insulinotropic polypeptide receptor gene and overexpressed in adrenals of patients with Cushing's syndrome.

The best characterized effect of glucose-dependent insulinotropic polypeptide (GIP) is its stimulatory effect on insulin secretion by pancreatic beta-cells. Recently, it was demonstrated that some cases of primary adrenal Cushing's syndrome were secondary to the ectopic expression of non-mutated GIP receptor (GIP-R) in bilateral adrenal hyperplasias or unilateral adrenal adenomas, resulting in food-dependent steroidogenesis. Using a human multiple-expression tissue array, GIP-R was found to be expressed in a large number of human adult and fetal tissues, but not in the adrenal gland. The analysis of the promoter region of human (h) GIP-R gene revealed six consensus sequences important in regulating the reporter gene activity and capable of binding to Sp1 and Sp3 transcription factors. Data obtained by gene array and semi-quantitative RT-PCR showed an increase in the expression of Sp3 and CRSP9 (co-regulator of Sp1 transcription factor, subunit 9) in the adrenal adenomas or bilateral macronodular hyperplasias of patients with GIP-dependent Cushing's syndrome; they were, however, also increased in some patients with non-GIP-dependent cortisol-secreting adenomas or with ACTH-dependent Cushing's disease. This study represents the first step in our understanding of the mechanisms involved in the regulation of the expression of the hGIP-R gene.