Strength training increases insulin action in healthy 50- to 65-yr-old men

1994 ◽  
Vol 77 (3) ◽  
pp. 1122-1127 ◽  
Author(s):  
J. P. Miller ◽  
R. E. Pratley ◽  
A. P. Goldberg ◽  
P. Gordon ◽  
M. Rubin ◽  
...  
Keyword(s):  
Strength Training ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Insulin Infusion ◽  
Glucose Clamp ◽  
Oral Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Fasting Plasma ◽  
Plasma Insulin Levels

The insulin resistance associated with aging may be due, in part, to reduced levels of physical activity in the elderly. We hypothesized that strength training increases insulin action in older individuals. To test this hypothesis, 11 healthy men 50–63 yr old [mean 58 +/- 1 (SE) yr] underwent a two-step hyperinsulinemic-euglycemic glucose clamp with concurrent indirect calorimetry and an oral glucose tolerance test (OGTT) before and after 16 wk of strength training. The training program increased overall strength by 47% (P < 0.001). Fat-free mass (FFM; measured by hydrodensitometry) increased (62.4 +/- 2.1 vs. 63.6 +/- 2.1 kg; P < 0.05) and body fat decreased (27.2 +/- 1.8 vs. 25.6 +/- 1.9%; P < 0.001) with training. Fasting plasma glucose levels and glucose levels during the OGTT were not significantly lower after training. In contrast, fasting plasma insulin levels decreased (85 +/- 25 vs. 55 +/- 10 pmol/l; P < 0.05) and insulin levels decreased (P < 0.05, analysis of variance) during the OGTT. Glucose infusion rates during the hyperinsulinemic-euglycemic glucose clamp increased 24% (13.5 +/- 1.7 vs. 16.7 +/- 2.2 mumol.kg FFM-1.min-1; P < 0.05) during the low (20 mU.m-2.min-1) insulin infusion and increased 22% (55.7 +/- 3.3 vs. 67.7 +/- 3.9 mumol.kg FFM-1.min-1; P < 0.05) during the high (100 mU.m-2.min-1) insulin infusion. These increases were accompanied by a 40% increase (n = 7; P < 0.08) in nonoxidative glucose metabolism during the high insulin infusion. These results demonstrate that strength training increases insulin action and lowers plasma insulin levels in middle-aged and older men.

Pre- and postabsorptive insulin secretion in chronic decerebrate rats

1986 ◽  
Vol 250 (4) ◽  
pp. R539-R548 ◽  
Author(s):  
F. W. Flynn ◽  
K. C. Berridge ◽  
H. J. Grill
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Oral Glucose ◽  
Base Line ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Percent Change ◽  
Plasma Insulin Levels

Basal, taste-stimulated (preabsorptive), and postabsorptive insulin secretion and plasma glucose responses were studied in chronic decerebrate rats and their pair-fed neurologically intact controls. In experiment 1, preabsorptive insulin responses (PIR) elicited by oral infusions of glucose solution was measured in chronic decerebrate rats. Oral glucose was ingested and led to a significant short-latency elevation in plasma insulin levels. Plasma glucose levels remained constant during this time. These data show that caudal brain stem mechanisms, in isolation of the forebrain, are sufficient for the neurally mediated PIR elicited by oral glucose stimulation. In experiment 2, effects of decerebration on postabsorptive insulin secretion were measured. During the 3 h immediately after transection there was no effect of decerebration on peripheral plasma insulin or glucose levels. Thereafter, however, basal plasma insulin levels of decerebrate rats were at least twice that of control rats. Plasma glucose levels of both groups remained identical despite the hyperinsulinemia in decerebrate rats. Atropine treatment decreased, and phentolamine administration elicited a greater absolute and percent change increase in insulin levels of decerebrate rats. These data indicate that altered autonomic tone contributes to maintaining the basal hyperinsulinemia in the decerebrate rat. In response to intragastric meals and glucose and intravenous glucose administration, insulin secretion was greater in decerebrate than in control rats. Percent change in insulin levels from base line was similar in both groups after intragastric meals and intravenous glucose. In response to intragastric glucose, however, percent increase in insulin levels was greater in decerebrate rats. Decerebrate rats demonstrated mild glucose intolerance after intragastric and intravenous treatments. These results are contrasted with the known effects of ventromedial hypothalamic lesions on insulin secretion and glucose homeostasis.

Intracisternal insulin alters sensitivity to CCK-induced meal suppression in baboons

1986 ◽  
Vol 250 (5) ◽  
pp. R856-R860 ◽  
Author(s):  
D. P. Figlewicz ◽  
L. J. Stein ◽  
D. West ◽  
D. Porte ◽  
S. C. Woods
Keyword(s):  
Food Intake ◽  
Plasma Insulin ◽  
Insulin Infusion ◽  
Meal Size ◽  
Immunoreactive Insulin ◽  
Gut Peptides ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Total Food Intake ◽  
Single Meal

We have previously reported that intravenous administration of the octapeptide of cholecystokinin (CCK-8) is more effective in reducing single meal size in baboons at noontime than in the morning. We have also reported that immunoreactive insulin levels in the cerebrospinal fluid (CSF) are elevated after animals have recently eaten. To test whether elevated CSF insulin levels can alter the efficacy of intravenous CCK to reduce meal size we administered subthreshold doses of CCK-8 to baboons infused with either synthetic CSF or CSF and insulin (100 microU X kg-1 X day-1) via the cisterna magna. Intravenous CCK-8 alone reduced 30-min meal size from 504 +/- 121 to 378 +/- 113 kcal (n = 7, P = NS). Chronic intracisternal insulin infusion enhanced CCK-8's suppressive effects such that 30-min meal size was reduced from 544 +/- 74 to 240 +/- 108 kcal (n = 7, P less than 0.005). Intracisternal insulin infusion had no significant effect on total food intake, basal plasma insulin and glucose levels, or postprandial plasma insulin and glucose levels. These findings suggest that central insulin may contribute to food intake regulation by modulating the ability of brain-gut peptides to alter single meal size.

Insulin modulates glucose-dependent insulinotropic polypeptide (GIP) secretion from enteroendocrine K cells in rats

2011 ◽  
Vol 392 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Nigel Irwin ◽  
Jacqueline M.E. Francis ◽  
Peter R. Flatt
Keyword(s):  
Plasma Glucose ◽  
Oral Glucose ◽  
Glucose Lowering ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Elevated Glucose ◽  
Plasma Insulin Levels ◽  
Glucose Plasma ◽  
And Control ◽  
Intestinal Weight

Abstract Effects of insulin excess and deficiency on glucose-dependent insulinotropic polypeptide (GIP) was examined in rats following insulinoma transplantation or streptozotocin (STZ) administration. Over 14 days, food intake was increased (p<0.001) in both groups of rats, with decreased body weight (p<0.01) in STZ rats. Non-fasting plasma glucose levels were decreased (p<0.01) and plasma insulin levels increased (p<0.001) in insulinoma-bearing rats, whereas STZ treatment elevated glucose (p<0.001) and decreased insulin (p<0.01). Circulating GIP concentrations were elevated (p<0.01) in both animal models. At 14 days, oral glucose resulted in a decreased glycaemic excursion (p<0.05) with concomitant elevations in insulin release (p<0.001) in insulinoma-bearing rats, whereas STZ-treated rats displayed similar glucose-lowering effects but reduced insulin levels (p<0.01). GIP concentrations were augmented in STZ rats (p<0.05) following oral glucose. Plasma glucose and insulin concentrations were not affected by oral fat, but fat-induced GIP secretion was particularly (p<0.05) increased in insulinoma-bearing rats. Exogenous GIP enhanced (p<0.05) glucose-lowering in all groups of rats accompanied by insulin releasing (p<0.001) effects in insulinoma-bearing and control rats. Both rat models exhibited increased (p<0.001) intestinal weight but decreased intestinal GIP concentrations. These data suggest that circulating insulin has direct and indirect effects on the synthesis and secretion of GIP.

Letters to the Editor

PEDIATRICS ◽  
1968 ◽  
Vol 42 (2) ◽  
pp. 371-372
Author(s):  
Marvin Cornblath ◽  
Allan Drash
Keyword(s):  
Islet Cell ◽  
Plasma Insulin ◽  
Letters To The Editor ◽  
Cell Adenoma ◽  
Insulin Levels ◽  
Fasting Plasma ◽  
Portal Plasma ◽  
Plasma Insulin Levels

In reply to Dr. Ehrlich's questions, we only wish that life would be as simple as he implied. The association of increased peripheral venous insulin values with islet cell adenoma is by no means universal in adults. In a child with multiple islet cell adenomata (Pediatrics, 39:59, 1967) , fasting plasma insulins as well as those following glucose, tolbutamide, and leucine, were not abnormally elevated. No other studies of peripheral or portal plasma insulin levels in infants or children with islet cell adenoma are known to us.

PLASMA-INSULIN LEVELS DURING ORAL GLUCOSE LOADS IN PREDIABETIC SUBJECTS

The Lancet ◽  
1973 ◽  
Vol 301 (7813) ◽  
pp. 1182
Author(s):  
Klaus Johansen ◽  
Erol Cerasi ◽  
Suad Efendić ◽  
Rolf Luft ◽  
AndrewL. Taylor
Keyword(s):  
Plasma Insulin ◽  
Oral Glucose ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Swim training alters sympathoadrenal and endocrine responses to hemorrhage in borderline hypertensive rats

1995 ◽  
Vol 269 (1) ◽  
pp. R124-R130
Author(s):  
D. E. McCoy ◽  
J. E. Steele ◽  
R. H. Cox ◽  
R. L. Wiley
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Rest Period ◽  
Endocrine Function ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Plasma Insulin Levels ◽  
Positive Correlations

Swim training alters cardiovascular, sympathoadrenal, and endocrine responses to hemorrhage in borderline hypertensive rats (BHR). The effects of 10, 20, and 30% blood volume hemorrhages on cardiovascular, sympathoadrenal, and endocrine function in swim-trained (T; 2 h/day, 5 day/wk for 10-12 wk) and age-matched, untrained, sedentary, control (UT) borderline hypertensive rats (BHR) were assessed. Heart rate (HR) in UT BHR was significantly greater during the baseline (rest) period than T BHR. HR increased slightly from baseline in both groups after 10% hemorrhage but was significantly decreased in both groups after 20 and 30% hemorrhages. The decrease was eliminated by atropine (1 mg/kg iv). Systolic (SBP) and diastolic (DBP) blood pressures decreased significantly after 20 and 30% hemorrhages in both T and UT BHR but were not different between the groups at these times. Plasma norepinephrine levels were significantly increased above baseline after 20 and 30% hemorrhages in UT BHR and were significantly greater in UT BHR than T BHR after 30% hemorrhage. Plasma glucose levels increased significantly after 30% hemorrhage in both groups but were significantly greater in UT BHR than T BHR. Both plasma norepinephrine and plasma epinephrine levels showed strong positive correlations with plasma glucose. After 20 and 30% hemorrhages, plasma insulin levels were unchanged in T BHR but were significantly decreased in UT BHR. Plasma insulin levels were significantly less in UT than T BHR after 30% hemorrhage. These results suggest that swim training alters the effect that hemorrhage exerts on endocrine and sympathoadrenal function in BHR.(ABSTRACT TRUNCATED AT 250 WORDS)

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