scholarly journals Hyperinsulinaemia increases insulin action in vivo in white adipose tissue but not in muscles

1990 ◽  
Vol 272 (1) ◽  
pp. 255-257 ◽  
Author(s):  
F Takao ◽  
M C Laury ◽  
A Ktorza ◽  
L Picon ◽  
L Pénicaud

The effect of 4 days of stable hyperglycaemia and resulting hyperinsulinaemia on insulin-induced glucose utilization by individual rat tissues was studied in vivo. The treatment produced a net increase in the glucose utilization index under both basal and insulin-stimulated (euglycaemic/hyperinsulinaemic clamp) conditions in white adipose tissue. On the contrary, glucose utilization was unchanged in aerobic muscles but was decreased in glycolytic skeletal muscles during the clamp.

1990 ◽  
Vol 267 (1) ◽  
pp. 99-103 ◽  
Author(s):  
I Cusin ◽  
J Terrettaz ◽  
F Rohner-Jeanrenaud ◽  
B Jeanrenaud

The effects of hyperinsulinaemia imposed on normal rats on the subsequent insulin-responsiveness in vivo of 2-deoxy-D-glucose uptake of white adipose tissue and of various muscle types were investigated. This was done by treating normal rats with insulin via osmotic minipumps, and by comparing them with saline-infused controls. Hyperinsulinaemia produced by prior insulin treatment resulted in a well-tolerated hypoglycaemia. At the end of the treatment, the glucose utilization index of individual tissues was determined by euglycaemic/hyperinsulinaemic clamps associated with the labelled 2-deoxy-D-glucose method. Prior insulin treatment resulted in increased insulin-responsiveness of the glucose utilization index of white adipose tissue, and in increased total lipogenesis in white adipose tissue and fat-pad weight. In contrast, prior insulin treatment resulted in a decreased glucose utilization index of several muscles. These opposite effects of hyperinsulinaemia on glucose utilization in white adipose tissue and muscles persisted when the hypoglycaemia-induced catecholamine output was prevented (adrenomedullectomy, propranolol treatment), as well as when hypoglycaemia was normalized by concomitant insulin treatment and glucose infusion. Insulin suppressed hepatic glucose production during the clamps in insulin-treated rats as in the respective controls, whereas total hepatic lipid synthesis and liver fat content were greater in rats treated with insulin than in controls. It is concluded that hyperinsulinaemia itself could be one of the driving forces responsible for producing increased glucose utilization by white adipose tissue, increased total lipid synthesis with fat accumulation in adipose tissue and the liver, together with an insulin-resistant state at the muscular level.


1988 ◽  
Vol 254 (3) ◽  
pp. E342-E348 ◽  
Author(s):  
S. Krief ◽  
R. Bazin ◽  
F. Dupuy ◽  
M. Lavau

In vivo whole-body glucose utilization and uptake in multiple individual tissues were investigated in conscious 30-day-old Zucker rats, which when obese are hyperphagic, hyperinsulinemic, and normoglycemic. Whole-body glucose metabolism (assessed by [3-3H]glucose) was 40% higher in obese (fa/fa) than in lean (Fa/fa) rats, suggesting that obese rats were quite responsive to their hyperinsulinemia (140 vs. 55 microU/ml). In obese compared with lean rats, tissue glucose uptake (assessed by the 2-deoxyglucose technique) was increased by 15, 12, and 6 times in dorsal, inguinal, perigonadal white depots, respectively; multiplied by 2.5 in brown adipose tissue; increased by 50% in skin from inguinal region but not in that from cranial, thoracic, or dorsal area; and increased twofold in diaphragm but similar in heart, in proximal intestine, and in total muscular mass of limbs. Our data establish that in young obese rats the hypertrophied white adipose tissue was a major glucose-utilizing tissue whose capacity for glucose disposal compared with that of half the muscular mass. Adipose tissue could therefore play an important role in the homeostasis of glucose in obese rats in the face of their increased carbohydrate intake.


1989 ◽  
Vol 257 (2) ◽  
pp. E255-E260 ◽  
Author(s):  
L. Penicaud ◽  
M. F. Kinebanyan ◽  
P. Ferre ◽  
J. Morin ◽  
J. Kande ◽  
...  

Euglycemic-hyperinsulinemic clamps coupled with an injection of [2-3H]deoxyglucose were performed in rats 1 or 6 wk after lesion of the ventromedial hypothalamus (VMH) and their age-matched controls. In the basal state, glucose utilization was not different in controls and VMH rats in all the tissues studied except in white adipose tissue where it was greatly increased after the lesion. When insulinemia was clamped at 850 microU/ml, glucose utilization was less important in glycolytic and normal in oxidative muscles in animals 1 wk after the lesion (VMH1) compared with controls. In animals 6 wk after the lesion (VMH6), all the muscles utilized less glucose than those of controls. In white adipose tissue, glucose utilization was increased twice more in VMH1 and returned to normal in VMH6. These data demonstrate a progressive development of insulin resistance in muscles. Simultaneously, there is a transient insulin hypersensitivity in white adipose tissue. This, together with a hypersecretion of insulin, could contribute to the development of body fat mass by redirecting glucose towards adipose tissue.


1994 ◽  
Vol 267 (6) ◽  
pp. E892-E899 ◽  
Author(s):  
M. C. Sugden ◽  
R. M. Grimshaw ◽  
H. Lall ◽  
M. J. Holness

The effects of food restriction (limited access to food for 2 h/day for 10 days) on lipoprotein lipase (LPL) activities and rates of fatty acid synthesis and glucose utilization in vivo in two superficial (interscapular and subcutaneous) and three deep abdominal white adipose tissue depots (parametrial, perirenal, and mesenteric) of adult female Wistar rats were examined before and at 2 h after a standard laboratory diet meal (5 g). Fasting LPL activities in perirenal (1.6-fold), mesenteric (5.9-fold), and subcutaneous (2.7-fold) adipose tissue, when expressed per unit of delipidated tissue, were increased in response to food restriction. This effect was retained (but not enhanced) after the meal. In contrast, muscle LPL activities were either unchanged or suppressed by food restriction. Stimulation of adipose tissue fatty acid synthesis and glucose utilization evoked by feeding in control rats was greatly enhanced by prior food restriction. There was no relationship between anatomical location and presence or absence of the response of adipose tissue LPL activity to food restriction, but the effect of food restriction to enhance the responses of fatty acid synthesis and glucose utilization to a meal was more marked in perirenal and parametrial adipose tissue than in the more superficial depots. The results thus demonstrate regional specificity in the response of adipose tissue functions to food restriction.


1991 ◽  
Vol 260 (4) ◽  
pp. E561-E567 ◽  
Author(s):  
M. Kergoat ◽  
M. Guerre-Millo ◽  
M. Lauva ◽  
B. Portha

The effect of chronic moderate insulin deficiency on in vivo insulin action was studied in young rats after neonatal (day of birth) streptozotocin (n0-STZ model) at a time (4 wk) when basal hyperglycemia is not yet established. The insulin action was quantified in vivo during insulin-glucose clamps performed on anesthetized rats while in the postabsorptive state; under basal or hyperinsulinemic conditions, total glucose production and utilization were assessed with a [3- 3H]-glucose perfusion, and local glucose utilization was estimated by measuring 2-deoxy-D-[1-3H]glucose 6-phosphate accumulation in various tissues. Compared with controls, the 4-wk-old n0-STZ rats were normoglycemic and hypoinsulinemic (P less than 0.05). The basal glucose production rate in the diabetics was significantly greater (P less than 0.05). During the clamp studies, suppression of endogenous glucose production by submaximal (1 nmol/l) or maximal (30 nmol/l) hyperinsulinemia was similar in both groups. Overall glucose utilization in the diabetics was significantly higher in the basal state and, after submaximal or maximal hyperinsulinemia, it remained significantly greater (P less than 0.001) than the corresponding utilization in the controls. This was correlated with an increased stimulation of glucose utilization in soleus muscle, diaphragm, white adipose tissue, and brown adipose tissue. In vitro studies using inguinal adipocytes showed that the glucose oxidative pathway retained normal sensitivity to insulin in the n0-STZ rats while the glucose conversion into lipids was significantly higher at sub-maximal insulin concentration compared with the control group.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 228 (1) ◽  
pp. 103-110 ◽  
Author(s):  
P Ferré ◽  
A Leturque ◽  
A F Burnol ◽  
L Penicaud ◽  
J Girard

A quantitative method allowing determination of glucose metabolism in vivo in muscles and white adipose tissue of the anaesthetized rat is presented. A tracer dose of 2-deoxy[3H]glucose was injected intravenously in an anaesthetized rat and the concentration of 2-deoxy[3H]glucose was monitored in arterial blood. After 30-80 min, three muscles, the soleus, the extensor digitorum longus and the epitrochlearis, periovarian white adipose tissue and brain were sampled and analysed for their content of 2-deoxy[3H]glucose 6-phosphate. This content could be related to glucose utilization during the same time period, since (1) the integral of the decrease of 2-deoxy[3H]glucose in arterial blood was known and (2) correction factors for the analogue effect of 2-deoxyglucose compared with glucose in the transport and phosphorylation steps were determined from experiments in vitro. Glucose utilization was then measured by this technique in the tissues of post-absorptive rats in the basal state (0.1 munit of insulin/ml of plasma) or during euglycaemic-hyperinsulinaemic glucose clamp (8 munits of insulin/ml of plasma) and of 48 h-starved rats. Results corresponded qualitatively and quantitatively to the known physiological characteristics of the tissues studied.


1987 ◽  
Vol 252 (2) ◽  
pp. E183-E188 ◽  
Author(s):  
A. F. Burnol ◽  
P. Ferre ◽  
A. Leturque ◽  
J. Girard

Glucose utilization rate has been measured in skeletal muscles, white adipose tissue, and mammary gland of anesthetized nonlactating and lactating rats. During lactation, basal glucose utilization is decreased by 40% in periovarian white adipose tissue and by 65% in epitrochlearis and extensor digitorum longus but not in soleus muscle. This may be related to the lower blood glucose and plasma insulin concentrations observed during lactation. Basal glucose utilization rate in the mammary gland was, respectively, 18 +/- 2 and 350 +/- 50 micrograms/min in nonlactating and lactating rats. During the euglycemic hyperinsulinemic clamp, a physiological increment in plasma insulin concentration (231 +/- 18 in lactating vs. 306 +/- 24 microU/ml in nonlactating rats) induces a similar increase in glucose utilization rate in skeletal muscles (except soleus) and white adipose tissue in the two groups of rats. Furthermore this low increase in plasma insulin concentration does not alter mammary glucose utilization rate in nonlactating rats but induces the same increase (sevenfold over basal) as a maximal insulin concentration in lactating rats. These data show that the active mammary gland is the most insulin-sensitive tissue of the lactating rat that has been tested. The overall increase in insulin sensitivity and responsiveness that has been described in lactating rats can then mainly be attributed to the presence of the active mammary gland.


2002 ◽  
Vol 10 (6) ◽  
pp. 555-558 ◽  
Author(s):  
Michael Boschmann ◽  
Götz Krupp ◽  
Friedrich C. Luft ◽  
Susanne Klaus ◽  
Jens Jordan

1995 ◽  
Vol 268 (3) ◽  
pp. R744-R751 ◽  
Author(s):  
T. G. Youngstrom ◽  
T. J. Bartness

When Siberian hamsters are transferred from long summerlike days (LDs) to short winterlike days (SDs) they decrease their body weight, primarily as body fat. These SD-induced decreases in lipid stores are not uniform. Internally located white adipose tissue (WAT) pads are depleted preferentially of lipid, whereas the more externally located subcutaneous WAT pads are relatively spared. These data suggest a possible differential sympathetic neural control over catecholamine-induced lipolysis and that lipolytic rates are greater for internal vs. external WAT pads. Moreover, if these differential rates of lipolysis are due to differential sympathetic nervous system (SNS) drives on the pads, then fat pad-specific catecholaminergic innervation may exist. Therefore, we tested whether inguinal WAT (IWAT; an external pad) and epididymal WAT (EWAT; an internal pad) were innervated differentially. In addition, we tested whether norepinephrine (NE) turnover (TO) reflected the presumed greater SNS drive on EWAT vs. IWAT after SD exposure. Injections of fluorescent tract tracers [Fluoro-Gold or indocarbocyanine perchlorate (DiI)] demonstrated projections from the SNS ganglia T13-L3 to both fat pads. Retrograde labeling revealed a relatively separate pattern of distribution of labeled neurons in the ganglia projecting to each pad. In vivo anterograde transport of DiI resulted in labeling in both IWAT and EWAT that included staining around individual adipocytes and occasionally retrogradely labeled cells. The proportionately greater decrease in EWAT compared with IWAT mass after 5 wk of SD exposure was reflected in greater EWAT NE TO than found in their LD counterparts for this pad.(ABSTRACT TRUNCATED AT 250 WORDS)


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