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Anthony L McCall

Publications and source records attributed to Anthony L McCall.

10 recordsLinked to original sources
PubMed2006

A novel analytical method for assessing glucose variability: using CGMS in type 1 diabetes mellitus.

BACKGROUND: Marked blood glucose (BG) fluctuations may increase the risk of some complications associated with diabetes. Acute BG excursions are common in patients with diabetes, but are not usually quantified, nor can they be captured by glycosylated hemoglobin level. This study evaluated the sensitivity of novel analytical methods for assessing BG variability using CGMS (Medtronic Minimed, Northridge, CA) data from patients treated with pramlintide, a drug that acutely reduces postprandial hyperglycemia when added to insulin therapy. METHODS: Retrospective analyses were done on 24-h CGMS profiles obtained from 22 evaluable subjects with type 1 diabetes using insulin pumps and receiving preprandial three times daily injections of placebo (n = 6) or 30 microg of pramlintide (n = 16) for 4 weeks. CGMS data were recorded at baseline, after 4 weeks of treatment, and after 2 weeks off-treatment. Three parameters were calculated for each time period: variability (BG rate of change), an index for severe hypoglycemia [low BG index (LBGI)], and an index for marked hyperglycemia [high BG index (HBGI)]. RESULTS: The mean postprandial BG rate of change was significantly lower after 4 weeks of pramlintide treatment compared with placebo treatment (0.87 vs. 1.21 mg/dL/min, P < 0.01) without changes in average glycemia, illustrating the sensitivity of this parameter to medication effects. The HBGI and LBGI indicated a decreased risk of hyperglycemia without a significant increase in risk of hypoglycemia after 4 weeks of pramlintide. CONCLUSIONS: These results suggest the potential utility of several novel methods for assessing variability and glycemic extremes to gauge the effects of pharmacological interventions not captured by glycosylated hemoglobin.

Adult↗
PubMed2005

Altered glycemia and brain-update and potential relevance to the aging brain.

Hyperglycemia characterizes diabetes mellitus and is linked to its chronic and acute complications. Cognitive dysfunction in diabetes occurs especially in longstanding disease and with poor glycemic control. Recent data in humans suggests that hyperglycemia causes acute cognitive dysfunction. The underlying mechanisms are unknown but deserve further research as diabetes is becoming epidemic and will likely contribute increasingly to premature cognitive decline. The primary side effect of diabetes treatment is hypoglycemia, particularly resulting from insulin treatment. CNS adaptations to acute and chronic hypoglycemia underlie the inability of some people to promptly recognize and defend against the risk of serious hypoglycemia. Data from human and animal models may help explain how altered glycemia affects brain function both acutely and chronically. Improved mechanistic understanding of altered glycemia's effects could prevent the adverse impact of diabetes upon the CNS and give new insights into effects that may exist in normal aging.

Aging↗
PubMed2004

Cerebral glucose metabolism in diabetes mellitus.

The brain uses glucose as its primary fuel. Cerebral metabolism of glucose requires transport through the blood-brain barrier, glycolytic conversion to pyruvate, metabolism via the tricarboxylic acid cycle and ultimately oxidation to carbon dioxide and water for full provision of adenosine triphosphate (ATP) and its high-energy equivalents. When deprived of glucose, the brain becomes dysfunctional or can be even permanently damaged. Glucose is stored as glycogen within astrocytes with potential importance for tolerance of hypoglycemia. Glycogen may also be important for the metabolic response to somatosensory stimulation and coupling of blood flow and cellular metabolism. Uncontrolled diabetes has a variety of adverse effects upon brain metabolism and function. Many aspects of function that affect the brain may be indirectly linked to cerebral glucose metabolism. Neurotransmitter metabolism, cerebral blood flow, blood-brain barrier and microvascular function may all be affected to varying degrees by either hypoglycemia or uncontrolled diabetes mellitus.

Animals↗
PubMed2004

Hypertension management in patients with diabetic nephropathy.

Treatment of hypertension, to reverse and delay proteinuria progression and kidney failure, is the primary focus of medical management in patients with diabetic nephropathy. The initial choice for hypertension treatment in those with early nephropathy involves agents that block the renin-angiotensin system. However, it is not clear what the best choices for further drug therapy management are, because there are few data concerning the impact that antihypertensive drug combinations have on hard clinical outcomes, such as preventing the need for dialysis, and death. Patients usually require several drugs for controlling hypertension, which becomes harder to control as nephropathy progresses. In this review, it is suggested that quantitatively tracking proteinuria to guide therapy and a broad focus on the cardiovascular and renal end points are important for best outcomes in patients. Strategies may vary based on stage of disease, comorbidities, and age. Therapies not directed specifically at hypertension may also significantly aid hypertension management in prevention of progressive nephropathy, comorbidities, and mortality.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

GLUT8 glucose transporter is localized to excitatory and inhibitory neurons in the rat hippocampus.

Fluorescence immunohistochemistry was performed to characterize the distribution and phenotype of GLUT8-positive neurons in rat brain and to compare the cellular distribution of GLUT8 with GLUT3 in the hippocampus. Based upon the absence of co-localization with the non-neuronal markers GFAP (astroglial) and OX42 (microglial), it appears that GLUT8 is expressed exclusively in neurons. At the cellular level, GLUT8 immunofluorescence was localized to neuronal cell bodies and the most proximal dendrites of inhibitory and excitatory neurons while GLUT3 immunofluorescence was localized to the neuropil in the hippocampus. These results demonstrate that GLUT8 is a neuron-specific glucose transporter expressed in the neuronal cell bodies of excitatory and inhibitory neurons in the rat hippocampus.

Animals↗