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Biomedical subjects

F Perez-Jimenez

Publications and source records attributed to F Perez-Jimenez.

25 records · Page 2Linked to original sources
PubMed1986

Interaction between marginal zinc deficiency and chronic alcoholism: pancreatic structure and function in rats in vitro.

The present study was done to determine interaction of ethanol and marginal zinc nutriture on morphology and function of rat pancreas. Sprague-Dawley rats were maintained on Wayne Rodent-Blox ad libitum; marginal zinc-deficient diet plus ethanol ad libitum and pair fed with animals fed marginal zinc-deficient liquid diet and zinc-supplemented liquid diet with ethanol for 33 (+/- 1 SEM) days. Body, pancreas, liver, heart, and kidney weights were determined, and studies of pancreatic DNA, RNA, total proteins and newly labeled proteins, amylase, lipase, trypsinogen, and chymotrypsinogen were done on pancreatic lobules in vitro. Ethanol feeding independent of the zinc content of the diet caused a decrease in zinc content of the liver, body weight, liver and pancreas weight, pancreatic DNA, total protein, and amylase concentration and an increase in lipase and trypsinogen concentrations and in secretion of amylase and lipase. Interaction of the marginal zinc diet and ethanol feeding resulted in a decreased synthesis of RNA and secretion of newly synthesized protein and an increase in secretion of serine proteases. Morphological studies revealed a reduction in the number of zymogen granules in animals fed low levels of zinc, also with an accumulation of lipid droplets when the diet contained ethanol. These studies confirmed our previous observations of specific injury to the pancreas due to marginal zinc nutriture or to ethanol, independent of each other. Marginal zinc nutriture in concert with ethanol resulted in impaired RNA synthesis and secretion of nascent proteins and increased secretion of serine proteases. These data indicate that altered zinc metabolism induced by ethanol per se may contribute to ethanol-induced disturbance of pancreatic function.

Alcoholism↗
PubMed1983

Lack of induction of serum gamma-glutamyltransferase in diabetes mellitus.

Some authors have suggested that carbohydrates can induce hepatic microsomal enzymes, resulting in increased serum gamma-glutamyltransferase (GGT) in diabetes mellitus. Previously we demonstrated the lack of serum GGT increases in patients with acute diabetic crises. In this work we studied serum GGT activity, blood glucose levels and glycosylated hemoglobin levels (HB A1) in 35 patients with diabetes mellitus and 27 healthy volunteers. We did not see differences in the serum GGT activity among controlled (25.05 +/- 2.72 U/l) and uncontrolled (26.44 +/- 4.05 U/l) diabetics and the control group (22.51 +/- 2.95 U/l). Also, there was no significant correlation between serum GGT and HB A1 levels in diabetic patients (r = 0.279). We think that our observations may be relevant because they support the hypothesis that hyperglycemia does not act as an enzyme-inducing agent in chronically uncontrolled diabetics and, furthermore, they indicate that in the presence of abnormal serum GGT levels in diabetics it is necessary to investigate other associated diseases.

Acyltransferases↗
PubMed1981

Selective IgA deficiency and the HLA-B8 antigen. Report of two cases with familial data.

Two patients had IgA deficiency, giardiasis, and the HLA-B8 antigen. The family of patient 1 included members with juvenile-onset diabetes mellitus, adrenal insufficiency, pernicious anemia, and hypothyroidism, a combination of unusual diseases that has been reported previously to occur as a syndrome with IgA deficiency and the HLA-B8 antigen. This coincidence makes it likely that these two patients and the one family previously described have a common pathogenic base, the inheritance of an abnormal immune-response gene that is acquired with the HLA-B8 antigen as a result of genetic dysequilibrium.

Adult↗