scholarly journals Pancreatic Insulinoma Presenting with Postprandial Hypoglicemias

2012 ◽  
Vol 19 (1) ◽  
pp. 99-103
Author(s):  
A. Florentiu ◽  
R. Barbu ◽  
M. Mitrache ◽  
R. Militaru ◽  
N. Georgescu ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Oral Glucose ◽  
Prolonged Fasting ◽  
Glucose Loading ◽  
Pancreatic Tail ◽  
Fasting Test ◽  
Pancreatic Insulinoma ◽  
Magnetic Resonance Scan ◽  
Fasting Hypoglycemia

Pancreatic Insulinoma Presenting with Postprandial HypoglicemiasWe report the case of an obese 58 years old patient evaluated for hypoglycemia. The response to a prolonged fasting test was normal, but symptomatic hypoglycemia ensued after mixed meals and with oral glucose loading. A magnetic resonance scan of the abdomen revealed a pancreatic tail tumor, histologically diagnosed as benign insulinoma after successful laparotomy. "Glucose-responsive" insulinomas, although rare, have been previously described in the literature. Therefore, the diagnosis of insulinoma should also be considered in patients that exhibit postprandial rather than fasting hypoglycemia.

Induction of renal phosphoenolpyruvate carboxykinase mRNA: suppressive effect of glucose

1989 ◽  
Vol 257 (1) ◽  
pp. F145-F151
Author(s):  
A. S. Pollock
Keyword(s):  
Metabolic Acidosis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Suppressive Effect ◽  
Oral Glucose ◽  
Prolonged Fasting ◽  
Glucose Loading ◽  
Glucose Administration ◽  
Liver And Kidney ◽  
Gluconeogenic Enzyme ◽  
Effect Of Glucose

The mRNA for the important gluconeogenic enzyme phosphoenolpyruvate carboxykinase (GTP) (PEPCK; EC 4.1.1.32) is expressed in liver and kidney. In the kidney, acidosis is a unique and potent stimulus, whereas insulin, the major counterregulatory hormone of gluconeogenesis, has no effect. In this study, we find that oral glucose administration to rats rapidly decreases the abundance of renal PEPCK mRNA by 50–72%. This reduction takes place in normal euglycemic, in insulin-induced hypoglycemic, and in streptozotocin-induced hyperglycemic diabetic animals. The effect of glucose is not seen in the presence of metabolic acidosis, whether induced by NH4Cl or by prolonged fasting. Therefore, it appears that oral glucose loading is a physiological suppressor of renal PEPCK message abundance, although not in acidosis.

Hepatic glycogen in humans. I. Direct formation after oral and intravenous glucose or after a 24-h fast

1989 ◽  
Vol 257 (2) ◽  
pp. E145-E157 ◽  
Author(s):  
J. Radziuk
Keyword(s):  
Glucose Infusion ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Metabolic Clearance ◽  
Glucose Load ◽  
Fasting Period ◽  
Intravenous Glucose ◽  
Glucose Loading ◽  
Constant Rate ◽  
Direct Formation

The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the double tracer method. [3–3H]glucose is infused at a constant rate for the determination of the metabolic clearance of glucose. [1–14C]glucose is administered with the glucose load. One hour after absorption or the intravenous glucose infusion is terminated, a glucagon infusion is initiated to mobilize the glycogen labeled with [1-14C]glucose and formed during the absorptive period. At this time a third tracer, [6-3H]glucose, is administered to measure glucose clearance. It was found that after the 12-h fast and oral glucose loading 7.2 +/- 1.1 g of hepatic glycogen appears to be formed directly from glucose compared with 8.4 +/- 1.0 g after the same load and a 24-h fast and 8.5 +/- 0.4 g after a 12-h fast and an equivalent intravenous glucose infusion. When the amount of label ([14C]glucose) mobilized that was not corrected for metabolic recycling was calculated, the data suggested that the amount of glycogen formed by gluconeogenic pathways was probably at least equal to that formed by direct uptake. It was also approximately 60% greater after a 24-h fast. It can be concluded that the amount of hepatic glycogen formed directly from glucose during glucose loading is not significantly altered by the route of entry or the extension of the fasting period to 24 h. The data suggest, however, that gluconeogenetic formation of glycogen increases with fasting.

Cellular Phosphate Shifts During Oral Glucose Loading

1992 ◽  
Vol 38 (11) ◽  
pp. 2338-2339 ◽  
Author(s):  
G J Kemp ◽  
A Blumsohn ◽  
B W Morris
Keyword(s):  
Oral Glucose ◽  
Glucose Loading

scholarly journals The effect of hGH deficiency on the insulin response to glucagon after oral glucose loading

Diabetologia ◽  
1977 ◽  
Vol 13 (5) ◽  
pp. 447-450 ◽  
Author(s):  
Z. Laron ◽  
M. Mimouni ◽  
Z. Josefsberg ◽  
Z. Zadik ◽  
M. Doron
Keyword(s):  
Insulin Response ◽  
Oral Glucose ◽  
Glucose Loading

Multiple hemangiomas involving the vertebral column

2005 ◽  
Vol 46 (5) ◽  
pp. 510-513 ◽  
Author(s):  
N. I. Sainani ◽  
S. A. Pungavkar ◽  
D. P. Patkar ◽  
M. A. Lawande ◽  
M. Naik
Keyword(s):  
Magnetic Resonance ◽  
Vertebral Column ◽  
Soft Tissue Tumors ◽  
Neurological Deficits ◽  
Local Pain ◽  
Magnetic Resonance Scan ◽  
Almost All ◽  
Slow Growing ◽  
Extensive Involvement ◽  
Indian Male

Hemangiomas are benign, slow-growing skeletal and soft tissue tumors that commonly involve the bony spine. When found in the spine, they are usually asymptomatic, but can sometimes be associated with local pain and/or neurological deficits. We report the case of a middle-aged Indian male with multiple hemangiomas involving almost all the vertebrae contiguously from C2 to S1 vertebral levels. These were discovered incidentally when a magnetic resonance scan was performed for backache. To the best of our knowledge, such extensive involvement of the spine has not been reported previously.

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