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Biomedical subjects

Robert P Hoffman

Publications and source records attributed to Robert P Hoffman.

8 recordsLinked to original sources
PubMed2006

Antecedent hypoglycemia does not alter increased epinephrine-induced lipolysis in type 1 diabetes mellitus.

Type 1 diabetic subjects have decreased epinephrine responses to hypoglycemia that may be counterbalanced by increased beta-adrenergic sensitivity. The goal of this study was to determine whether type 1 diabetic subjects have increased metabolic response to epinephrine and to determine the effect of antecedent hypoglycemia on these responses. Muscular glucose uptake across the forearm (forearm glucose uptake, Fick principle) and lipolysis (free fatty acid and glycerol levels) were studied before and during a 4-hour euglycemic, hyperinsulinemic (40 mU x m(-2) x min(-1)) clamp with epinephrine infusion (0.015 microg x kg(-1) x min(-1)) over 3 hours. Subjects were studied twice, once with antecedent hypoglycemia (2.8 mmol/L for two 2-hour sessions) and once with antecedent euglycemia (5 mmol/L) the day prior. Free fatty acid and glycerol concentrations were higher, and total body glucose utilization and forearm glucose uptake during epinephrine were lower in diabetic than in control subjects (P < .05). Antecedent hypoglycemia had no effect. These results demonstrate that type 1 diabetic subjects have increased lipolysis and decreased glucose utilization in response to epinephrine. These effects are not altered by antecedent hypoglycemia.

Adolescent↗
PubMed2004

Pubertal changes in HOMA and QUICKI: relationship to hepatic and peripheral insulin sensitivity.

BACKGROUND: Homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) are measures of insulin resistance and insulin sensitivity derived from fasting glucose (FG) and insulin levels. They thus should reflect, in principle, insulin action on both the liver and the periphery. METHODS: Twenty-three prepubertal and early pubertal adolescents were studied at baseline and after 6 months, using the frequently sampled intravenous glucose tolerance test (IVGTT) with labeled glucose. Total body insulin sensitivity (SI) was calculated using the minimal model and total glucose concentrations. Peripheral insulin sensitivity (SI*) was calculated from labeled glucose concentrations. Hepatic insulin resistance (HIR) was calculated by multiplying glucose production over the last hour by the average insulin level. HOMA and QUICKI were calculated from the fasting glucose and insulin values. RESULTS: HOMA, QUICKI fasting insulin, and glucose to insulin ratio were all significantly related to SI (p <0.05) but were not independently related to SI* or HIR. Multiple linear regression analysis revealed that both SI* and HIR independently predicted HOMA and fasting glucose (p <0.1). QUICKI, fasting insulin, and glucose to insulin ratio were not independently related to SI, SI*, or HIR. CONCLUSIONS: HOMA and fasting insulin reflect total body insulin sensitivity and HIR but not peripheral insulin sensitivity in prepubertal and early pubertal adolescents.

Blood Glucose↗
PubMed2004

Practical management of type 1 diabetes mellitus in adolescent patients: challenges and goals.

Type 1 diabetes mellitus in adolescents presents diagnostic and management challenges. Diagnostically, the challenge is to distinguish type 1 from type 2 diabetes. A thin adolescent in diabetic ketoacidosis is easily recognized as having type 1 diabetes. However, since obesity does not negate the presence of type 1 diabetes, it is appropriate to measure diabetes-related antibody, C-peptide, and insulin levels in individuals who are thought to have type 2 diabetes to ensure that they do not have type 1 or a mixed type of diabetes. The goals for the management of type 1 diabetes in adolescents are to (i) prevent diabetic ketoacidosis; (ii) prevent severe hypoglycemia; (iii) maintain normal growth and development; and (iv) prevent long-term diabetic complications. To prevent diabetic ketoacidosis, patients must take their insulin appropriately. To ensure that this happens, increased parental supervision, psychological counseling, or placement in a different home environment may be necessary. All patients must be taught to appropriately manage sick days and test their urine for ketones when hyperglycemia is present. Prevention of severe hypoglycemia involves ensuring that the patient understands the symptoms of hypoglycemia and knows to test and treat it when the signs are present. Patients and families also need to know how to adjust insulin doses to prevent hypoglycemia and how to manage exercise appropriately. Patients with hypoglycemic unawareness need to meticulously avoid hypoglycemia. To maintain normal growth and development, adolescents with type 1 diabetes must have the appropriate tools to effectively match their meals to their lifestyle and to avoid the increased weight gain associated with improved glycemic control without intentionally manipulating their insulin dose to lose weight. The Diabetes Control and Complications Trial demonstrated that improved glycemic control decreased the risk of long-term diabetic complications. The goals of treatment in this study should be the goals for all adolescents with type 1 diabetes. To reach these goals, home glucose monitoring is critical. Patients need to know how to adjust insulin to maintain glucose levels in the range of 70-120 mg/dL (3.9-6.7 mmol/L) before meals. Insulin regimens need to be individually tailored to meet each patient's needs. Patients should be followed in a clinic using a multidisciplinary team approach at least every 3 months. Glycosylated hemoglobin should be measured at each visit. Regular eye exams, blood pressure monitoring, and urinary microalbumin measurements are critical. In this manner, the goals of management of type 1 diabetes in adolescents can be met.

Adolescent↗
PubMed2002

Adolescent adherence in type 1 diabetes.

Adolescents with Type 1 diabetes have poorer glycemic control and more hypoglycemia than do adults. While physiologic reasons for these problems exist, the most common problems are failure to administer insulin, monitor glucose levels, and maintain an appropriate meal plan.

Adolescent↗
PubMed2002

Comparison of insulin sensitivity and glucose effectiveness determined by the one- and two-compartment-labeled minimal model in late prepubertal children and early adolescents.

Multiple methods are used to determine insulin sensitivity. Most commonly used in children are euglycemic-hyperinsulinemic clamp and frequently sampled intravenous glucose tolerance (FSIVGTT) with minimal modeling (MinMod). The parameters S(G) and S(I) of MinMod are related to insulin sensitivity and glucose effectiveness, respectively, but inappropriate modeling of glucose kinetics causes inaccuracies. Glucose tracer use may mitigate such inaccuracies, allowing use of multiple modeling approaches, including a 2-compartment model (2CMM). This study was designed to compare the 1-compartment model (1CMM) and 2CMM in a pediatric population. Twenty-three children were studied 4 times using FSIVGTT with [6,6] D(2) glucose. Glucose effectiveness and insulin sensitivity were calculated by 1CMM (S*(G1) and S*(I1)) and 2CMM (S*(G2) and S*(I2)). Indices were reliably estimated in 86 of 87 tests for 1CMM, but only in 49 for 2CMM. S*(G1) overestimated S*(G2), but they were positively related. S*(I1) and S*(12) were not different and were positively related. This suggests that inadequate modeling by the 1CMM has a smaller impact on glucose tolerance indices in children than in adults. Comparison with classical MinMod gave results analogous to those in adults (MinMod S(G) was larger than S*(G1), MinMod S(I) was smaller than S*(I1)). These results demonstrate significant differences in glucose effectiveness, but not insulin sensitivity, as measured by 1CMM and 2CMM in early adolescents. Thus, when insulin sensitivity is the primary interest, the 1CMM is more robust because its parameters are more reliably estimated than those of 2CMM and is the logical choice in pediatric population-based studies.

Child↗
PubMed2002

Systemic and local adrenergic regulation of muscle glucose utilization during hypoglycemia in healthy subjects.

Adrenergic responses are crucial for hypoglycemic recovery. Epinephrine increases glucose production, lipolysis, and peripheral insulin resistance as well as blood flow and glucose delivery. Sympathetic activation causes vasoconstriction and reduces glucose delivery. To determine the effects of alpha- and beta-adrenergic activity on muscle glucose uptake during hypoglycemia, we studied forearm blood flow (FBF) (plethysmography), arteriovenous glucose difference (AV-diff), and forearm glucose uptake (FGU) during insulin infusion with 60 min of euglycemia followed by 60 min of hypoglycemia. Twelve healthy subjects (27 plus minus 5 years of age) were randomized to intravenous propranolol (IV PROP, 80 microg/min), intravenous phentolamine (IV PHEN, 500 microg/min), intra-arterial propranolol (IA PROP, 25 microg/min), intra-arterial phentolamine (IA PHEN, 12 microg/min per 100 ml forearm tissue), and saline (SAL). FBF increased during hypoglycemia with SAL (P < 0.001) but not with IA or IV PROP. FGU (P = 0.015) and AV-diff (P = 0.099) fell during hypoglycemia with IA PROP but not with IV PROP. FBF increased during hypoglycemia with IA and IV PHEN (P < 0.005). AV-diff fell during hypoglycemia with IA and IV PHEN (P < 0.01), but FGU was unchanged. Blood pressure fell (P < 0.001), and adrenergic and neuroglycopenic symptoms increased with IV PHEN (P < 0.01). Thus, systemic but not local propranolol prevents a decrease in forearm glucose extraction during hypoglycemia, suggesting that epinephrine increases peripheral muscular insulin resistance through systemic effects. alpha-Adrenergic activation inhibits vasodilation and helps maintain brain glucose delivery.

Adrenergic alpha-Antagonists↗