Search PubMed⌕ Search

Biomedical subjects

R R Henry

Publications and source records attributed to R R Henry.

108 records · Page 6Linked to original sources
PubMed1986

Metabolic consequences of very-low-calorie diet therapy in obese non-insulin-dependent diabetic and nondiabetic subjects.

To determine the effects of very-low-calorie diets on the metabolic abnormalities of diabetes and obesity, we have studied 10 obese, non-insulin-dependent diabetic (NIDDM) and 5 obese, nondiabetic subjects for 36 days on a metabolic ward during consumption of a liquid diet of 300 kcal/day with 30 g of protein. Rapid improvement occurred in the glycemic indices of the diabetic subjects, with mean (+/- SEM) fasting plasma glucose falling from 291 +/- 21 to 95 +/- 6 mg/dl (P less than 0.001) and total glycosylated hemoglobin from 13.1 +/- 0.7% to 8.8 +/- 0.3% (P less than 0.001) (normal reference range 5.5-8.5%). Lipid elevations were normalized with plasma triglycerides reduced to less than 100 mg/dl and total plasma cholesterol to less than 150 mg/dl in both groups. Hormonal and substrate responses were also comparable between groups with reductions in insulin and triiodothyronine and moderate elevations in blood and urinary ketoacid levels without a corresponding rise in free fatty acids. Electrolyte balance for sodium, potassium, calcium, and phosphorus was initially negative but approached equilibrium by completion of the study. Magnesium, in contrast, remained in positive balance in both groups throughout. Total nitrogen loss varied widely among all subjects, ranging from 70 to 367 g, and showed a strong positive correlation with initial lean body mass (N = 0.83, P less than 0.001) and total weight loss (N = 0.87, P less than 0.001). The nondiabetic group, which had a significantly greater initial body weight and lean body mass than the diabetic group, also had a significantly greater weight loss of 450 +/- 31 g/day compared with 308 +/- 19 g/day (P less than 0.01) in the diabetic subjects. The composition of the weight lost at completion was similar in both groups and ranged from 21.6% to 31.3% water, 3.9% to 7.8% protein, and 60.9% to 74.5% fat. The contribution of both water and protein progressively decreased and fat increased, resulting in unchanged caloric requirements during the diet. This study demonstrates that short-term treatment with a very-low-calorie diet in both obese diabetic and nondiabetic subjects results in: safe and effective weight loss associated with the normalization of elevated glucose and lipid levels, a large individual variability in total nitrogen loss determined principally by the initial lean body mass, and progressive increments in the contribution of fat to weight loss with stable caloric requirements and no evidence of a hypometabolic response.

Adult↗
PubMed1986

Effects of weight loss on mechanisms of hyperglycemia in obese non-insulin-dependent diabetes mellitus.

To quantitate the effects of weight loss on the mechanisms responsible for hyperglycemia in non-insulin-dependent diabetes mellitus (NIDDM), eight obese subjects with NIDDM were studied before and after weight reduction with posttreatment assessment after 3 wks of isocaloric (weight maintenance) refeeding. After weight loss of 16.8 +/- 2.7 kg (mean +/- SE), the fasting plasma glucose level decreased 55% from 277 +/- 21 to 123 +/- 8 mg/dl. The individual fasting glucose levels were highly correlated with the elevated basal rates of hepatic glucose output (HGO) (r = 0.91, P less than .001), which fell from 138 +/- 11 to 87 +/- 5 mg X m-2 X min-1 after weight loss. The change in fasting plasma glucose also correlated significantly with the change in the basal rates of HGO (r = 0.74, P less than .05). This was associated with reduced fasting serum levels of glucagon (from 229 +/- 15 to 141 +/- 12 pg/ml), reduced free fatty acids (from 791 +/- 87 to 379 +/- 35 mu eq/L), and unchanged basal insulin levels (17 +/- 4 to 15 +/- 2 microU/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

3-O-Methylglucose↗
PubMed1985

Glycemic effects of intensive caloric restriction and isocaloric refeeding in noninsulin-dependent diabetes mellitus.

To assess the effects of very low caloric (VLC) diets on glucose homeostasis in noninsulin-dependent diabetes mellitus, 30 obese subjects with NIDDM were studied for 40 days while eating a 330 Cal/day diet, with a subgroup of 12 subjects further evaluated during 40 days of refeeding. All subjects successfully lost weight, with an average weight loss of 4.6 +/- 0.2 kg (+/- SEM) after 10 days, 7.1 +/- 0.3 kg after 20 days, and 10.5 +/- 0.4 kg after 40 days of VLC diet therapy. Thus, weight loss was steady and progressive throughout the diet period. In contrast, the majority (87%) of the reduction in mean fasting plasma glucose (FPG) levels (297 +/- 13 to 158 +/- 10 mg/dl; P less than 0.001) occurred after 10 days of VLC diet therapy, with a further reduction in glucose levels to 138 +/- 9 mg/dl on day 40. The FPG response measured after 10 days of VLC diet was unrelated to the degree of obesity, rate or extent of weight loss, or prevailing insulin levels, but did correlate significantly with the initial FPG level (r = 0.37; P less than 0.05) and duration of diabetes (r = 0.42; P less than 0.05). After discontinuation of the VLC diet and refeeding of an isocaloric (weight maintenance) diet in 12 subjects, a variable increase in the FPG occurred, with an average increase of 80% after 40 days of refeeding. However, the mean FPG level after 40 days of refeeding was still markedly lower than that before VLC diet therapy (254 +/- 20 vs. 167 +/- 14 mg/dl; P less than 0.02) despite withdrawal of antidiabetic medication in all subjects. The basal hepatic glucose output (HGO) fell rapidly from 149 +/- 13 to 81 +/- 5 mg/M2 X min (P less than 0.001) after 10 days of VLC diet and rose from 67 +/- 4 to 88 +/- 7 mg/M2 X min (P less than 0.001) after 10 days of refeeding. Basal HGO demonstrated a highly significant positive correlation with FPG levels (r = 0.89; P less than 0.001) before and during both VLC diet therapy and refeeding. A significant correlation was also found between the change in FPG level and the change in basal HGO (r = 0.84; P less than 0.001) during both VLC diet and refeeding. Compared to that before the VLC diet, glucose tolerance to mixed meals was markedly improved during the refeeding period, with no change in circulating insulin levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Insulin resistance in non-insulin dependent (type II) and insulin dependent (type I) diabetes mellitus.

Insulin resistance is a characteristic feature of non-insulin dependent diabetes mellitus (NIDDM) due to target tissue defects in insulin action. Abnormalities of cellular insulin action can be divided into receptor and post-receptor defects. Patients with impaired glucose tolerance are insulin resistant due to decreased insulin receptors resulting in decreased insulin sensitivity and rightward shifted in vivo dose response curves. Patients with NIDDM are insulin resistant due to a combination of receptor and post-receptor defects. The greater the severity of the diabetes (greater fasting hyperglycemia) the greater the post-receptor defect, and in those patients with more significant fasting hyperglycemia the post-receptor defect is the predominant abnormality leading to the insulin resistant state. At least one of the abnormalities underlying this post-receptor defect involves a decrease in glucose transport system activity in freshly isolated adipocytes. This defect in glucose transport, is not expressed in cultured fibro-blasts, indicating that the abnormality in glucose disposal seen in vivo and in glucose transport seen in freshly isolated cells is an acquired phenomenon. Consistent with this, the post-receptor defect is partially reversible by insulin therapy, which leads to a 50-70% reversal of the reduced rates of in vivo glucose disposal and in vitro glucose transport. Insulin resistance also exists in poorly controlled IDDM patients, due to a postreceptor defect in insulin action. This insulin resistance is not present in well controlled IDDM patients, and is completely reversible when poorly controlled patients are treated with intensive insulin therapy. Insulin is produced in the pancreatic beta cell as the primary biosynthetic product preproinsulin. This peptide is rapidly converted to proinsulin (MW approximately 9000). Proinsulin is converted to insulin (MW approximately 6000) plus C-peptide in the secretory granule with a small amount (approximately 5 percent) of the proinsulin remaining unconverted. After a brief time in the peripheral circulation (half-life six to 10 minutes), insulin interacts with target tissues to exert its biologic effects. One of insulin's major biologic effects is the promotion of overall glucose metabolism, and abnormalities of this aspect of insulin action can lead to a number of important clinical and pathophysiologic states including Type II diabetes, also known as non-insulin-dependent diabetes mellitus (NIDDM). Since insulin travels from the beta cell through the circulation to the target tissues, abnormalities at any of these loci can influence the ultimate action of the hormone. These abnormalities, all

Diabetes Mellitus↗
PubMed1983

Susceptibility of inbred mice to Leishmania tropica infection: correlation of susceptibility with in vitro defective macrophage microbicidal activities.

Eleven mouse strains were inoculated in footpads with amastigotes of Leishmania tropica and observed for 12 weeks. Liver and spleen impression smears from infected mice were examined for the presence of intracellular parasites. Four strains (BALB/cJ, C57L/J, NZW/N, and P/J) failed to heal the subcutaneous lesion and showed evidence of systemic infection; the remaining seven strains (A/J, C3H/HeJ, C3H/HeN, C3HeB/FeJ, C57BL/6J, C57BL/10J, and C57BL/10ScN) were each resistant to infection and resolved their lesions by Week 10. Macrophages from the four susceptible strains could not be activated to kill L. tropica amastigotes by treatment with soluble lymphocyte products in vitro. In contrast, macrophages from all seven resistant strains responded to lymphokine treatment and eliminated 80-90% of intracellular parasites. These results suggest that in vitro macrophage microbicidal activities predict the course of systemic leishmanial disease.

Animals↗
PubMed1981

Hypothyroidism, triiodothyronine antibodies, and hyperprolactinemia.

This report describes the development of triiodothyronine (T3) antibodies in a patient with Hashimoto's thyroiditis that resulted in compensated hypothyroidism and hyperprolactinemia. The patient, a 23-year-old woman, had a small goiter, modest elevation of thyrotropin (TSH) and prolactin (PRL) levels, and a markedly elevated T3 level. Circulating antibodies to T3 were demonstrated that presumably rendered the T3 physiologically inactive. Saturation of antibody binding sites by incremental dosages of liothyronine (triiodothyronine) sodium (12.5 to 87.5 microgram/day) resulted in normalization of both the TSH and PRL levels.

Adult↗
PubMed1979

Mass balance: a quantitative guide to clinical nutritional therapy. II. The dialyzed patient.

The concepts of mass balance are extended to the nutritional management of the patient with chronic renal failure on dialysis. The use of these concepts permits estimation of protein catabolism from calculated rates of urea generation, using measurement of blood urea levels. Protein catabolic rate will equal intake in the stable patient (zero nitrogen balance), allowing for accurate nutritional screening in a large dialysis population for whom these values are available without individual dietary surveys. This has resulted in a four-fold reduction in routine monitoring of protein nutrition in such patients, freeing the dietitian to concentrate on specific problems. These concepts also comprise a key aspect of the National Cooperative Dialysis Study which seeks to maintain BUN at different levels in four carefully controlled modes of dialysis therapy. With these methods, the monitoring and control of BUN and protein intake has made the dietitian a pivotal member of this study staff.

Blood Urea Nitrogen↗
PubMedDate not supplied

Duck immune responses to Riemerella anatipestifer vaccines.

Riemerella anatipestifer (Ra) infection is probably the most economically important infectious disease of farm ducks worldwide but the immune responses to natural infection and vaccines are poorly understood. We have used the lymphocyte transformation test (LTT) to study the expression of cell-mediated immunity (CMI), and the enzyme-linked immunosorbent assay to monitor antibody (Ab) production following administration of formalin-inactivated and live attenuated serotype 2 (= G) Ra vaccines. Lymphocytes (8x10(5) in 200 microl of RPMI + 10% duck serum, in 96 well trays) were stimulated with Ra antigen, prepared by freeze-thaw and sonication; optimum responses were obtained with antigen at 6.25 microg/ml. Cells were cultured for 3 days at 41.6 degrees C/5% CO(2), prior to assessing 3H-thymidine uptake. Ra bacterin, incorporating aluminium hydroxide as adjuvant, stimulated strong but transient (about 4 weeks) LTT response; there was some cross-reaction of the LTT to proteins derived from other serotypes of Ra. Revaccination stimulated slightly stronger responses with the same time course. The Ab response to each vaccination was longer-lived than the LTT response. Vaccination with a live, attenuated strain of Ra stimulated weaker but longer lasting LTT responses, but similar Ab responses compared to the bacterin. It is apparent, therefore, that the transient protection reported using Ra bacterins is due to the fact that the CMI response to these vaccines is transient; and that it is possible for ducks to have detectable levels of serum Ab at times when CMI is not detectable by LTT. These observations are important in terms of our understanding of immunopathogenesis, immunoprophylaxis, and immunodiagnosis in Ra.

Aluminum Hydroxide↗
PubMedDate not supplied

Metabolic consequence of two-week fructose feeding in diabetic subjects.

We studied the metabolic effects of 2-wk fructose feeding as the sweetener in the diet of seven non-insulin-dependent diabetic individuals. The data demonstrated reduced postprandial hyperglycemia to an oral glucose challenge after 14 days without a significant difference in insulin response. There was no change in the markedly blunted glucose response to a fructose challenge but a significantly lower insulin response (area under the 3-h curve) was observed after 14 days of fructose feeding. There was reduced postprandial hyperglycemia after 14 days of fructose feeding with test meals as compared with baseline, without significant differences in insulin response. We also found no significant difference in free fatty acids, cholesterol, high-density lipoprotein (HDL) cholesterol, pyruvate, lactate, or uric acid after fructose feedings. There was a 13% increase in triglyceride levels after 14 days in 5 subjects with initial fasting hypertriglyceridemia (greater than 150 mg/dl). Insulin receptor binding to isolated adipocytes did not change after 14 days of fructose feeding.

Adipose Tissue↗
PubMedDate not supplied

Role of glycemic control and protein restriction in clinical management of diabetic kidney disease.

OBJECTIVE: To assess the role of control of blood glucose levels and restriction of dietary protein in the management of diabetic nephropathy. METHODS: We summarize the results of pertinent published studies of glycemic control and modification of protein intake to provide information about strategies that potentially could benefit patients with diabetes and renal dysfunction. RESULTS: Considerable evidence is available to support the contention that improved glycemic control may have beneficial effects on the development and progression of diabetic renal disease. Maximal benefits of improved glycemia occur when instituted before the onset of macroalbuminuria. Once overt diabetic nephropathy is established, improved glycemic control may not be beneficial. Current evidence indicates that a glycosylated hemoglobin level of less than 8.1% should be the glycemic goal. At this level, the risk of developing micro-albuminuria is substantially reduced, and the risk of hypoglycemia is minimized. Most studies have been conducted in type I diabetes, and the results have been extrapolated to type II diabetes. Whether improved glycemic control will be equally beneficial in the nephropathy of type II diabetes has yet to be determined. Although some scientific evidence supports dietary protein restriction in patients with diabetic nephropathy, the extent of restriction needed for optimal benefits and minimal side effects remains to be determined. On the basis of current information, patients with both types of diabetes who have evidence of nephropathy should have protein limited to the recommended dietary allowance for adults (0.8 g/kg of body weight per day or approximately 10% of total daily caloric intake), and protein should be derived primarily from vegetable and lean animal sources. CONCLUSION: End-stage renal disease is not inevitable in patients with diabetic nephropathy. Normalization of glucose levels and modification of protein intake can favorably influence the course of diabetes-related kidney disease.

Journal Article↗
PubMedDate not supplied

Combination therapy for type 2 diabetes.

OBJECTIVE: To discuss a rational approach to improvement of glycemic control in patients with type 2 diabetes mellitus with use of combination therapy. METHODS: We review the mechanisms of action and clinical applications for the various antidiabetic agents alone and in various combinations. Relevant studies in the literature are reviewed. RESULTS: Although diet and exercise remain the cornerstones of treatment, in most patients with type 2 diabetes, pharmacologic agents are needed to achieve optimal glycemic control and likely reduce the incidence of microvascular and possibly macrovascular complications as well. Sulfonylureas have long been the foundation of oral pharmacologic therapy and provide adequate glycemic control for most patients for 5 to 10 years or longer. In the past, when treatment with sulfonylureas was no longer effective, insulin therapy was inevitable. With the approval of several new pharmacologic agents for the treatment of type 2 diabetes, however, the addition of one or more orally administered agents to sulfonylurea therapy or use of other oral combination therapy is rapidly evolving as a means of optimizing glycemic control. In many patients, combination therapy can delay the need to add or switch to insulin, or it can enhance glycemic control in patients already receiving insulin. In selected patients treated solely with insulin, discontinuation of insulin treatment and reinitiation of oral therapy may even be possible. CONCLUSION: Currently, four classes of orally administered antidiabetic agents are available for use in patients with type 2 diabetes: insulin secretagogues, biguanides, a-glucosidase inhibitors, and thiazolidinediones. By taking advantage of differing mechanisms of action, combination therapy is evolving as a means of optimizing glycemic control in patients in whom a single agent or insulin is inadequate. Combinations of orally administered agents can often delay the need for insulin or in combination with insulin aid in achieving glycemic goals. Continuing research will help optimize combination therapies even further.

Journal Article↗
PubMedDate not supplied

Implantable insulin pump vs multiple-dose insulin for non-insulin-dependent diabetes mellitus: a randomized clinical trial. Department of Veterans Affairs Implantable Insulin Pump Study Group.

OBJECTIVE: To determine whether implantable insulin pump (IIP) therapy and multiple daily insulin (MDI) injections could equally attain improved blood glucose control, and to compare the 2 treatments with respect to reducing daily blood glucose fluctuations, reducing serious hypoglycemic insulin reactions, and improving patients' quality of life. DESIGN: Randomized clinical trial. SETTING: Seven Veterans Affairs medical centers. PATIENTS: One hundred twenty-one male type II diabetic patients between the ages of 40 and 69 years, receiving at least 1 injection of insulin per day and having hemoglobin A1c (HbA1c) levels of 8% or above. INTERVENTION: Intensive therapy (IIP or MDI) for 1 year. MAIN OUTCOME MEASURES: Hemoglobin A1c and blood glucose levels. RESULTS: Blood glucose levels declined to 7.96+/-1.08 mmol/L (143.4+/-19.5 mg/dL) and 8.30+/-1.52 mmol/L (149.6+/-27.4 mg/dL) (mean +/- SD) for IIP and MDI, respectively (P=.57). Hemoglobin A1c levels improved in both groups (time effect P<.001), to means of 7.54%+/-0.83% (MDI) vs 7.34%+/-0.79% (IIP). IIP reduced blood glucose fluctuations compared with MDI (P<.001), and reduced the incidence of mild clinical hypoglycemia by 68% (P<.001); IIP also eliminated the weight gain associated with MDI therapy and yielded better overall quality-of-life (P=.03) and impact-of-disease subscale scores (P=.05). Adverse events included 25% of subjects with episodes of insulin underdelivery due to microprecipitates of insulin within the pump. CONCLUSIONS: Intensive insulin therapy with IIP and MDI is effective in controlling non-insulin-dependent diabetes mellitus. IIP has significant advantages in reducing glycemic variability, clinical hypoglycemia, and weight gain, while improving aspects of quality of life.

Adult↗