PubMed Health⌕ Search

Biomedical subjects

B C Hansen

Publications and source records attributed to B C Hansen.

At least 19 recordsLinked to original sources
PubMed1992

Correlation between plasma beta-cell tropin concentrations and body weight in obese rhesus monkeys.

The fasting plasma concentration of the pituitary peptide beta-cell tropin [beta-CT, adrenocorticotropic hormone-(22-39)] was measured in 17 rhesus monkeys from a colony known to develop spontaneous obesity. The weight of the animals was 9.4-23.9 kg (12-46% body fat). Plasma beta-CT concentrations were 0.03-0.84 nmol/l and were strongly correlated with body weight (P = 0.014, r = 0.584). Plasma beta-CT was also correlated with plasma insulin concentration as a power function (P = 0.011, r = 0.600) and with percent body fat up to 40% (P = 0.003, r = 0.0804). Plasma insulin is also correlated with body weight (P = 0.015, r = 0.578) but does not decline when body fat is in excess of 40%, supporting the hypothesis that beta-CT may be involved in a feed-back control mechanism, perhaps mediated by insulin. Because beta-CT has been shown in rodent studies to be a potent insulin secretagogue and lipogenic agent, it is possible that beta-CT is causally involved in the development of obesity and that there may be central determinants of obesity mediated through pituitary secretion of beta-CT.

Adipose Tissue↗
PubMed1991

Insulin-like growth factor-I in non-insulin-dependent diabetic monkeys: basal plasma concentrations and metabolic effects of exogenously administered biosynthetic hormone.

Plasma insulin-like growth factor-I (IGF-I) concentrations and the effects of exogenous IGF-I administration were determined in 26 rhesus monkeys; each animal was well characterized regarding its degree of obesity, plasma glucose and insulin levels, and glucose tolerance (KG). Five separate groups were identified: lean normal, obese normoinsulinemic and normoglycemic, obese hyperinsulinemic with normal glucose tolerance, impaired glucose tolerant, and spontaneously diabetic (type II, non-insulin-dependent diabetes mellitus [NIDDM]). Basal plasma IGF-I levels in all monkeys ranged from 249 to 1,093 ng/mL and were strongly associated with age (r = -.66; P less than .001) and KG (r = .59; P less than .001), but not with body weight, body fat, or fasting plasma glucose or insulin levels. In addition, the acute insulin-like effects of exogenously administered IGF-I on glucose disappearance were studied in vivo in a dose-response comparison to insulin (subcutaneous administration of IGF-I at doses of 50, 100, or 200 micrograms/kg v insulin at 0.3 U/kg). Five hyperinsulinemic normoglycemic monkeys (fasting plasma glucose, 67 +/- 2 mg/dL; insulin, 163 +/- 42 microU/mL) and overt type II diabetic monkeys (fasting plasma glucose, 201 +/- 13 mg/dL; insulin, 38 +/- 6 microU/mL) each underwent a series of three to five experiments to determine the time course and degree of hypoglycemia induced by IGF-I as compared with insulin or with control (saline) injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Changes in lipoprotein concentrations during the development of noninsulin-dependent diabetes mellitus in obese rhesus monkeys (Macaca mulatta).

Abnormalities in plasma lipoprotein concentrations commonly found in subjects with noninsulin-dependent diabetes may be related to insulin resistance, hyperinsulinemia, hyperglycemia, or other metabolic defects. The middle-aged obese rhesus monkey is an animal model in which these defects can be separated in time during the development of diabetes. It is, therefore, a model system for examining the sequence of metabolic changes which occur before and after the onset of diabetes. This sequence of changes was used in the present study to determine if lipoprotein changes occur in association with the development of diabetes in the rhesus monkey. Increases in plasma triglyceride, very low density lipoprotein (VLDL) triglyceride, and VLDL cholesterol, and decreases in high density lipoprotein cholesterol were observed across previously identified groups ranging from normal to diabetic. Plasma triglycerides increased from 0.54 +/- 0.09 (normal) to 1.27 +/- 0.50, 1.93 +/- 0.79, and 4.28 +/- 2.24 in three intermediate groups with progressive hyperinsulinemia and insulin resistance, to 7.59 +/- 2.73 mmol/L in the diabetic monkeys. Increases in VLDL triglyceride and VLDL cholesterol paralleled the plasma triglyceride increases. High density lipoprotein cholesterol decreased across the groups from 2.33 +/- 0.16 (normal) to 1.72 +/- 0.20, 1.17 +/- 0.13, and 1.09 +/- 0.20 mmol/L in the intermediate groups, and was lowest in the diabetic monkeys, 1.00 +/- 0.21. The obese rhesus monkey can therefore be used to study lipoprotein abnormalities as they occur both before and in noninsulin-dependent diabetes.

Aging↗
PubMed1990

Low urinary chiro-inositol excretion in non-insulin-dependent diabetes mellitus.

BACKGROUND AND METHODS: Inositol is a major component of the intracellular mediators of insulin action. To investigate the possible role of altered inositol metabolism in non-insulin-dependent diabetes mellitus (NIDDM), we used gas chromatography and mass spectrometry to measure the myo-inositol and chiro-inositol content of urine specimens from normal subjects and patients with NIDDM: The study subjects were whites, blacks, and Pima Indians. The type of inositol and its concentration in insulin-mediator preparations from muscle-biopsy specimens from normal subjects and diabetic patients were also determined. RESULTS: The urinary excretion of chiro-inositol was much lower in the patients with NIDDM (mean [+/- SE], 1.8 +/- 0.8 mumol per day) than in the normal subjects (mean, 84.9 +/- 26.9 mumol per day; P less than 0.01). In contrast, the mean urinary myo-inositol excretion was higher in the diabetic patients than in the normal subjects (444 +/- 135 vs. 176 +/- 46 mumol per day; P less than 0.05). There was no correlation between chiro-inositol excretion and the age, sex, or weight of the diabetic patients, nor was there any correlation between urinary chiro-inositol and myo-inositol excretion in either group. The results were similar in a primate model of NIDDM, and chiro-inositol excretion was decreased to a lesser extent in animals with prediabetic insulin resistance. chiro-Inositol was undetectable in insulin-mediator preparations from muscle-biopsy samples obtained from patients with NIDDM: Similar preparations from normal subjects contained substantial amounts of chiro-inositol. Furthermore, the chiro-inositol content of such preparations increased after the administration of insulin during euglycemic-hyperinsulinemic-clamp studies in normal subjects but not in patients with NIDDM: CONCLUSIONS: NIDDM is associated with decreased chiro-inositol excretion and decreased chiro-inositol content in muscle. These abnormalities seem to reflect the presence of insulin resistance in NIDDM:

Age Factors↗
PubMed1990

Food intake and meal patterns in rhesus monkeys: significance of chronic hyperinsulinemia.

To investigate the role of plasma insulin on food intake, we have examined the effect of naturally occurring chronic hyperinsulinemia on the feeding behavior of male rhesus monkeys. Two groups of monkeys, a group with normal fasting insulin concentrations (52.4 +/- 2.2 microU/ml) (mean +/- SE) and a hyperinsulinemic group (148.6 +/- 14.5 microU/ml), were selected to be similar in weight, 13.0 +/- 1.0 and 15.3 +/- 0.5 kg, respectively, prior to study. Food intake and feeding patterns were recorded and analyzed. No differences in either daily caloric intake, 815.2 +/- 27.4 versus 890.0 +/- 64.2 kcal (p less than 0.32), or feeding patterns were found. The number of meals taken per day did not differ between the two groups, 8.7 +/- 1.7 versus 6.7 +/- 1.1 (p less than 0.35), nor did meal size differ, 129 +/- 16.5 versus 110.5 +/- 16.3 (p less than 0.45). We conclude that chronic endogenous hyperinsulinemia as it occurs naturally in some obese rhesus monkeys has no significant effect on daily feeding behavior.

Animals↗
PubMed1990

Postingestional effects of a high-protein diet on the regulation of food intake in monkeys.

Using a system in which the composition of an intragastric diet could be manipulated while oral factors were kept constant, we studied the effect of a high-protein diet on food intake. Four adult rhesus monkeys with chronically implanted intragastric cannulas were trained to use suction-activated food pumps that were monitored by computer so feeding pattern could be assessed over periods averaging 4 wk each. Each suck delivered the oral control diet while simultaneously activating a second pump, which delivered a second diet directly into the stomach, resulting in net diet compositions of either 14% or 50% protein. The calorie intake was consistently reduced by 24.7 +/- 1.6% when the high-protein diet was fed. The effect on intake was not due to increased diet osmolality. A doubling in plasma branched-chain amino acid concentration occurred when the high-protein diet was fed. These data indicate that feeding a high-protein diet results in a physiological appetite suppression, possibly mediated through branched-chain amino acids.

Amino Acids↗
PubMed1990

Beta-cell hyperresponsiveness: earliest event in development of diabetes in monkeys.

Diabetes develops spontaneously in some, but not all, obese middle-aged monkeys. Longitudinal study of spontaneously obese rhesus monkeys has now shown the separation in time of the onset of various abnormalities associated with non-insulin-dependent diabetes mellitus (NIDDM). Glucose tolerance and acute and late insulin release were assessed at 6-mo to 1-yr intervals over a period of 7 yr in six young, lean, normal animals and 14 middle-aged obese, initially normoglycemic monkeys. Over 2-5 yr, while under study, five of the obese subjects developed overt diabetes [fasting plasma glucose greater than 140 mg/dl and decreased glucose disappearance rates (KG) less than 1.5]. Progressively increasing hyperinsulinemia leading to a 10-fold increase in basal plasma insulin levels (mean +/- SE = 443 +/- 69 microU/ml) and a fivefold increase in insulin response to glucose occurred independent of degree of obesity and before hyperglycemia. Later, basal and stimulated insulin levels declined before significant hyperglycemia. We conclude that in the monkey beta-cell function is clearly enhanced, not reduced, in the earliest stages of the progression to NIDDM but is reduced just before overt diabetes.

Aging↗
PubMed1989

Hepatic glucose production and insulin sensitivity preceding diabetes in monkeys.

The purpose of this study was to identify the relationship between basal hepatic glucose production (HGP) and peripheral insulin sensitivity as assessed by the hyperinsulinemic euglycemic clamp prior to and during the development of non-insulin-dependent (type 2) diabetes mellitus in rhesus monkeys. Twenty-six male monkeys (Macaca mulatta), including normal animals and monkeys in various phases of the development of spontaneous obesity-associated type 2 diabetes were studied. Fasting plasma glucose (FPG) and insulin (FIRI), basal HGP using a [3H]glucose infusion, and peripheral insulin sensitivity (as determined by the euglycemic clamp technique) were examined. The earliest change that could be detected was a significant reduction in peripheral insulin sensitivity accompanied by increased FIRI. These changes preceded a significant deterioration of glucose tolerance. Basal HGP changed in parallel with FPG (r = 0.90, P less than 0.001), becoming significantly elevated only when FPG rose to levels diagnostic of diabetes (greater than 140 mg/dl). Thus basal HGP and fasting glucose levels showed no significant changes early in the development of type 2 diabetes. We conclude that the early serial decreases in insulin sensitivity and progressive increases in FIRI, with or without decreased glucose tolerance, are prognostic of the future development of diabetes in obese monkeys, a longitudinal process that is also likely to be observed in most if not all obese humans progressing to diabetes.

Animals↗
PubMed1989

Peripheral neuropathy in diabetic monkeys.

Peripheral neuropathy is a significant complication of human diabetes and a source of morbidity. Appropriate experimental models may aid in understanding its pathogenesis and in developing therapeutic strategies. We sought to determine whether spontaneously diabetic obese adult monkeys developed peripheral neuropathy and whether it occurred early or late in relation to the onset of hyperglycemia. We studied nerve conduction in both motor (peroneal, median, and ulnar) and sensory (median and ulnar) nerves in 13 adult male rhesus monkeys, 4 overtly diabetic and 9 nondiabetic (mean age 21 +/- 2 and 16 +/- 2 yr, respectively, NS; mean fasting plasma glucose 14.5 +/- 3.4 and 4.4 +/- 0.6 mM, P = .001). The diabetic animals had significantly reduced motor conduction velocities and prolonged F-wave latencies. Motor-evoked amplitudes did not differ. In the diabetic monkeys, nerve conduction times were increased in motor fibers, which could be identified as early as 2 yr after the onset of hyperglycemia. These abnormalities are similar to those seen in humans and suggest further study of these animals as a primate model of human diabetic neuropathy.

Animals↗
PubMed1988

Metabolic clearance rates of synthetic human growth hormone in lean and obese male rhesus monkeys.

The MCR of synthetic human GH was studied in eight adult male rhesus monkeys (Macaca mulatta). Four monkeys were lean (less than 20% body fat), and four were obese (greater than 35% body fat). The monkeys were given a single bolus injection of GH (2.5 micrograms/kg BW), followed by a constant infusion of GH (250 micrograms/h) for 2.5 h. Venous blood samples were collected before the infusion and every 10 min during the infusion. In both groups a plateau of the plasma GH concentrations, indicating a steady state, was reached 70 min after the start of the infusion. The MCR of GH was calculated from the ratio of the constant GH infusion rate and the plateau plasma GH concentration in each monkey. The MCR of synthetic GH was 12.7 +/- 1.7 (+/- SD) L/24 h in the lean group and 19.5 +/- 2.9 L/24 h in the obese group (P less than 0.007). However, the MCR/kg ratio in the lean monkeys was the same as that in the obese animals. We conclude that 1) MCR of GH is directly proportional to body weight; and 2) the lower plasma GH levels in obesity may be due to an increase in its MCR not compensated for by an appropriate increase in the rate of GH secretion.

Age Factors↗
PubMed1988

Dietary considerations for obese diabetic subjects.

Individuals with an upper-body form of obesity show greater associations with higher glucose excursions, exacerbated insulin resistance, increased abnormality of lipoprotein profile, and higher cardiovascular risk. Individuals with obesity and diabetes are at great risk for cardiovascular disease. Weight reduction and improvement in blood glucose control through dietary interventions for the obese person with non-insulin-dependent diabetes mellitus (NIDDM) hold the greatest potential for reducing morbidity and mortality. The relative merits of different weight-reduction programs are unclear, but regimens should be nutritionally complete, easy to follow, and include a program for maintaining the reduced weight level. Improvement in insulin action and the possibility of slowing development of clinical nephropathy or end-stage renal disease in NIDDM through weight loss have been found. Very low calorie diets, when used with medical supervision, may lead to significant weight loss, improved metabolic status, and even reduction or elimination of the need for oral hypoglycemic agents or insulin; however, further studies are needed to examine possible negative outcomes in people with NIDDM before very low calorie diets can be recommended. The causes of obesity and its connection with diabetes are unclear, but even modest calorie restriction may be beneficial to obese diabetic patients because of the positive effects on blood glucose levels and requirements for insulin and oral antidiabetic agents.

Body Weight↗
PubMed1988

Changes in insulin responses and binding in adipocytes from monkeys with obesity progressing to diabetes.

To gain insight into cellular events associated with the progression of obesity to diabetes, we have studied glucose metabolism and insulin responses in adipocytes from monkeys with spontaneous obesity. Over a 3- period, we studied animals which (A) remained relatively lean; (B) became obese (over 30 percent body fat) with normal glucose tolerance; (C) were obese and developed hyperinsulinemia (over 100 microU/ml); and (D) were obese and subsequently developed noninsulin-dependent diabetes (NIDDM) (fasting plasma glucose above 140 mg/dl and abnormal glucose tolerance test). Adipocyte glucose utilization, evaluated by conversion of 14-C-glucose to CO2 and lipids, was measured in the absence and presence of varying concentrations of insulin, using cells prepared from biopsy samples of subcutaneous abdominal fat. The major change in adipocyte metabolism was a decrease in basal and insulin-stimulated glucose utilization in NIDDM, relative to the enhanced responses observed in cells from the obese-hyperinsulinemic monkeys. Longitudinal studies of individual monkeys over 2-3 years led to the following additional observations regarding adipocyte glucose metabolism. Basal and insulin-stimulated glucose utilization dropped markedly as hyperinsulinemia progressed into diabetes. As impairments in glucose tolerance worsened in diabetes, adipocytes showed only a modest or negligible additional impairment in basal and insulin-stimulated glucose oxidation. Insulin binding was reduced in adipocytes from monkeys with obesity as compared to lean controls, and was similar in cells from monkeys with obesity and NIDDM. In the monkeys, obesity was initially associated with enhanced adipocyte metabolism. With the spontaneous development of NIDDM, glucose metabolism in adipocytes was depressed. The progression of metabolic events from hyperinsulinemia to NIDDM in monkeys includes cellular changes in insulin responses at the level of the adipocyte.

Adipose Tissue↗
PubMed1987

Effects of different heat treatments during processing of soybean meal on nursery and growing pig performance.

Four soybean meals (SBM) were manufactured in a commercial solvent-extraction plant to give a much wider range in heat treatment than is usually found among commercially available SBM. The SBM were designated in ascending order of heat treatment as Under, Normal, Over and Rumen Escape. The nutritive value of the four meals was evaluated in a series of five feeding trials using 458 pigs: two performance and two diet preference trials with pigs weaned at 4 wk of age and one performance trial with growing pigs (17.4 kg initial weight were conducted). In both nursery and grower trials, there were no differences (P greater than .10) in performance of pigs fed the four meals. However, in the nursery trials, the severely heated meal (Rumen Escape) supported slightly lower gains (6.4%) and less desirable feed efficiency (3.5%) than the average of the other three meals. Growing pig performance was essentially the same for all meals. This suggests that older pigs either used the Rumen Escape meal more effectively than nursery pigs, or the Rumen Escape diet contained adequate digestible lysine for 17.4-kg pigs to grow optimally. In the preference studies, pigs selected between Normal- and Rumen Escape-supplemented diets. Pigs consumed 63 and 62% of the Normal diet in preference trials 1 and 2, but these differences were not significant (P greater than .10) due to the large variation among pens. These data suggest that the range of heat treatment normally found among commercially available SBM (Under, Normal and Over meals) has no effect on the nutritive value of the meal for swine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗