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G G Singer

Publications and source records attributed to G G Singer.

42 records · Page 3Linked to original sources
PubMed1985

Can marked hyperglycemia occur without ketosis?

The significance of ketosis in this syndrome has been evaluated from several viewpoints. With respect to acid-base considerations (pH, anion gap), ketosis was not very significant. However, with respect to sustained hyperglycemia, the combustion of less glucose than normal by the brain is critical and it is likely that ketone body metabolism plays an important role in this regard. This point can be underscored by a quantitative example. First, assume that the maximum rate of new glucose production in a fasted subject is less than 100 g of glucose per day. Second, since the brain will burn 100 g of glucose per day in a non-ketotic subject, it follows that, even in the absence of glucosuria, there will be a net daily consumption of glucose. Since the hyperglycemic individual has only an extra 100 or so g of glucose, it follows that the blood glucose concentration would approach the renal threshold in several days in the absence of ketosis. Recall that this is a minimum estimate because glucose oxidation in other organs and glucosuria will remove an additional quantity of glucose. Hyperglycemia can only be maintained in the absence of glucose intake if there is a reduced rate of glucose metabolism in the brain. The brain can diminish its rate of glucose catabolism by several mechanisms, including a diminished metabolic rate in the brain and/or the consumption of non-glucose fuels (free fatty acids or beta-hydroxybutyrate) by this organ.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMedDate not supplied

Quantitative analysis of glucose loss during acute therapy for hyperglycemic hyperosmolar syndrome.

Four patients with severe hyperglycemia and hyperosmolality were studied to quantitate the major mechanisms responsible for the fall in blood glucose concentration. Insulin was not administered to any of these patients during the first 15 h of therapy. In each case, there was a fall in glucose concentration due to dilution; this was quantitated by chloride space analysis and accounted for 24-34% of the fall in concentration. The size of the glucose pool decreased for two reasons. Glucosuria accounted for the majority of the reduction in the size of the glucose pool in the patients with the smallest decrease in extracellular fluid (ECF) volume [and hence the best preserved glomerular filtration rate (GFR)]. In contrast, glucosuria was a less important factor in causing glucose loss in the patients with very low GFR values. The size of the glucose pool also decreased due to glucose metabolism that did not require exogenous insulin. Thus the fall in glucose concentration in the initial therapy in patients with the hyperglycemic hyperosmolar syndrome is multifactorial and is not absolutely dependent on exogenous insulin. Furthermore, the patients grouped in this diagnostic category represent a heterogeneous population with the common features of severe hyperglycemia, hyperosmolality, and a negative or weakly reactive test for serum ketones.

Adult↗
PubMedDate not supplied

The antigen presentation function of renal tubular epithelial cells.

Renal tubular epithelial cells (TEC) have the capacity to function as antigen-presenting cells (APC). The processing of native antigen and the presentation of peptides bound to major histocompatibility complex (MHC) class II products on TEC results in engagement of the T cell antigen receptor (TCR). TEC also express a variety of adhesion molecules and cytokines which may enhance their interaction with T cells. The expression of intercellular adhesion molecules (ICAM-1) and vascular cell adhesion molecules (VCAM-1) on TEC enhances their adherence to T cells. Immune-activated TEC display and/or secrete numerous cytokines including tumor necrosis factor alpha (TNF alpha) which may provide accessory signals for T cells and upregulate TEC adhesion molecule receptors. We review the two signals required for T cell activation and suggest a model whereby T cell interaction with TEC can have two possible sequelae: (1) T cell activation or (2) T cell unresponsiveness. TEC and other parenchymal cells could potentially be important in maintaining peripheral tolerance to tissue-specific self-antigens if Ia (signal 1) and costimulatory signals (signal 2) are not induced simultaneously. Conversely, coordinate expression of signals 1 and 2 would inevitably lead to organ-specific immune injury. Studies to further elucidate the nature of T cell interactions with parenchymal cells are clearly essential for a more complete understanding of the pathogenesis of autoimmunity.

Animals↗