PANCREATIC AND SERUM INSULIN IN THE NEW ZEALAND STRAIN OF OBESE MICE

1964 ◽  
Vol 28 (2) ◽  
pp. 163-172 ◽  
Author(s):  
J. G. T. SNEYD
Keyword(s):  
Adipose Tissue ◽  
New Zealand ◽  
Glucose Uptake ◽  
Serum Insulin ◽  
Porcine Insulin ◽  
Equivalent Amount ◽  
Obese Mice ◽  
Normal Controls ◽  
Stimulation Of ◽  
Insulin Like Activity

SUMMARY The insulin content of the pancreas and the insulin-like activity of the blood serum are considerably higher in mice of the New Zealand obese strain than in normal controls. The rate of glucose uptake by adipose tissue and hemi-diaphragms incubated in the absence of added insulin did not differ significantly in tissues from obese and normal mice and the stimulation of glucose uptake caused by addition of insulin was similar in tissues from the two strains. Insulin extracted from the pancreas of New Zealand obese mice stimulated glucose uptake by adipose tissue and muscle from obese mice to the same extent as an equivalent amount of porcine insulin.

Does hyperinsulinemia in ob/ob mice cause an insulin-stimulated adipose tissue?

1976 ◽  
Vol 230 (3) ◽  
pp. 602-607 ◽  
Author(s):  
EG Loten ◽  
Y Le Marchand ◽  
F Assimacopoulos-Jeannet ◽  
RM Denton ◽  
B Jeanrenaud
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Pyruvate Dehydrogenase ◽  
Serum Insulin ◽  
Acetyl Coa Carboxylase ◽  
Obese Mice ◽  
Lipogenic Enzymes ◽  
Insulin Stimulation ◽  
Endogenous Insulin ◽  
Stimulation Of

After a 1-h preincubation to remove endogenous insulin, adipose tissue of obese mice (C57BL/L4 ob/ob) had a lower rate of glucose metabolism than tissue which was not preincubated. In contrast, preincubation did not change the metabolism of adipose tissue from lean mice (C57B1/6J +/+). The preincubation effect was abolished in obese mice which had had their serum insulin levels lowered toward normal by streptozotocin treatment. Injection of anti-insulin serum to obese mice caused adipose tissue removed 15 min after the injection to display a rate of glucose metabolsim lower than that of tissue removed before the injection. No such effect was seen in lean mice. These data are consistent with the hypothesis that hyperinsulinemia in the obese mice causes a chronic state of insulin stimulation of their adipose tissue, possibly contributing to their high rates of lipogenesis and their obesity. Several lipogenic enzymes were measured in adipose tissue of both lean and obese mice, and no single enzymatic abnormality was detected which might explain the hyperlipogenesis. Pyruvate dehydrogenase and acetyl-CoA carboxylase were both insulin-sensitive enzymes in lean and obese mice.

Response of human adipose tissue to endogenous serum insulin-like activity in vitro

Metabolism ◽  
1967 ◽  
Vol 16 (1) ◽  
pp. 47-56 ◽  
Author(s):  
John A. Owen ◽  
Richard W. Lindsay ◽  
Joe H. Gaskin ◽  
Guy Hollifield
Keyword(s):  
Adipose Tissue ◽  
Serum Insulin ◽  
Human Adipose Tissue ◽  
Insulin Like Activity

scholarly journals Stimulation of glucose uptake in murine soleus muscle and adipocytes by 5-(4-phenoxybutoxy)psoralen (PAP-1) may be mediated by Kv1.5 rather than Kv1.3

2014 ◽  
Author(s):  
Robert A Ngala ◽  
Mohamed S Zaibi ◽  
Kenneth Langlands ◽  
Claire J Stocker ◽  
Jonathan RS Arch ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Soleus Muscle ◽  
White Adipose Tissue ◽  
Gastrocnemius Muscle ◽  
Obese Mice ◽  
Wild Type ◽  
High Concentration ◽  
White Adipocytes

Kv1 channels are shaker-related potassium channels that influence insulin sensitivity. Kv1.3 -/- mice are protected from diet-induced insulin resistance and some studies suggest that Kv1.3 inhibitors provide similar protection. However, it is unclear whether blockade of Kv1.3 in adipocytes or skeletal muscle increases glucose uptake. There is no evidence that the related channel Kv1.5 has any influence on insulin sensitivity and its expression in adipose tissue has not been reported. PAP-1 is a selective inhibitor of Kv1.3, with 23-fold, 32-fold and 125-fold lower potencies as an inhibitor of Kv1.5, Kv1.1 and Kv1.2 respectively. Soleus muscles from wild-type and genetically obese ob/ob mice were incubated with 2-deoxy[1-14C]-glucose for 45 min and formation of 2-deoxy[1-14C]-glucose-6-phosphate was measured. White adipocytes were incubated with D-[U-14C]-glucose for 1h. TNFalpha and Il-6 secretion from white adipose tissue pieces were measured by enzyme-linked-immunoassay. In the absence of insulin, a high concentration (3 μM) of PAP-1 stimulated 2-deoxy[1-14C]-glucose uptake in soleus muscle of wild-type and obese mice by 30% and 40% respectively, and in adipocytes by 20% and 50% respectively. PAP-1 also stimulated glucose uptake by adipocytes at the lower concentration of 1 μM, but at 300 nM, which is still 150-fold higher than its EC50 value for inhibition of the Kv1.3 channel, it had no effect. In the presence of insulin, PAP-1 (3 μM) had a significant effect only in adipocytes from obese mice. PAP-1 (3 μM) reduced the secretion of TNFalpha by adipose tissue but had no effect on the secretion of IL-6. Expression of Kv1.1, Kv1.2, Kv1.3 and Kv1.5 was determined by RT-PCR. Kv1.3 and Kv1.5 mRNA were detected in liver, gastrocnemius muscle, soleus muscle and white adipose tissue from wild-type and ob/ob mice, except that Kv1.3 could not be detected in gastrocnemius muscle, nor Kv1.5 in liver, of wild-type mice. Expression of both genes was generally higher in liver and muscle of ob/ob mice compared to wild-type mice. Kv1.5 appeared to be expressed more highly than Kv1.3 in soleus muscle, adipose tissue and adipocytes of wild-type mice. Expression of Kv1.2 appeared to be similar to that of Kv1.3 in soleus muscle and adipose tissue, but Kv1.2 was undetectable in adipocytes. Kv1.1 could not be detected in soleus muscle, adipose tissue or adipocytes. We conclude that inhibition of Kv1 channels by PAP-1 stimulates glucose uptake by adipocytes and soleus muscle of wild-type and ob/ob mice, and reduces the secretion of TNFalpha by adipose tissue. However, these effects are more likely due to inhibition of Kv1.5 than to inhibition of Kv1.3 channels.

scholarly journals MEASUREMENT OF SMALL QUANTITIES OF INSULIN-LIKE ACTIVITY WITH RAT ADIPOSE TISSUE. III. PERSISTENCE OF SERUM INSULIN-LIKE ACTIVITY AFTER PANCREATECTOMY*

1962 ◽  
Vol 41 (9) ◽  
pp. 1699-1707 ◽  
Author(s):  
Jurgen Steinke ◽  
Anna Sirek ◽  
Vilma Lauris ◽  
Francis D. W. Lukens ◽  
Albert E. Renold
Keyword(s):  
Adipose Tissue ◽  
Serum Insulin ◽  
Rat Adipose Tissue ◽  
Insulin Like Activity

scholarly journals Role of hypoxia in obesity-induced disorders of glucose and lipid metabolism in adipose tissue

2009 ◽  
Vol 296 (2) ◽  
pp. E333-E342 ◽  
Author(s):  
Jun Yin ◽  
Zhanguo Gao ◽  
Qing He ◽  
Dequan Zhou ◽  
ZengKui Guo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Interstitial Oxygen ◽  
Obese Mice ◽  
Cell Type Specificity

Recent studies suggest that adipose tissue hypoxia (ATH) may contribute to endocrine dysfunction in adipose tissue of obese mice. In this study, we examined hypoxia's effects on metabolism in adipocytes. We determined the dynamic relationship of ATH and adiposity in ob/ob mice. The interstitial oxygen pressure (Po2) was monitored in the epididymal fat pads for ATH. During weight gain from 39.5 to 55.5 g, Po2 declined from 34.8 to 20.1 mmHg, which are 40–60% lower than those in the lean mice. Insulin receptor-β (IRβ) and insulin receptor substrate-1 (IRS-1) were decreased in the adipose tissue of obese mice, and the alteration was observed in 3T3-L1 adipocytes after hypoxia (1% oxygen) treatment. Insulin-induced glucose uptake and Akt Ser473 phosphorylation was blocked by hypoxia in the adipocytes. This effect of hypoxia exhibited cell type specificity, as it was not observed in L6 myotubes and βTC6 cells. In response to hypoxia, free fatty acid (FFA) uptake was reduced and lipolysis was increased in 3T3-L1 adipocytes. The molecular mechanism of decreased fatty acid uptake may be related to inhibition of fatty acid transporters (FATP1 and CD36) and transcription factors (PPARγ and C/EBPα) by hypoxia. The hypoxia-induced lipolysis was observed in vivo after femoral arterial clamp. Necrosis and apoptosis were induced by hypoxia in 3T3-L1 adipocytes. These data suggest that ATH may promote FFA release and inhibit glucose uptake in adipocytes by inhibition of the insulin-signaling pathway and induction of cell death.

scholarly journals Insulin-stimulated glucose transport in muscle. Evidence for a protein-kinase-C-dependent component which is unaltered in insulin-resistant mice

1989 ◽  
Vol 258 (1) ◽  
pp. 141-146 ◽  
Author(s):  
J F Tanti ◽  
N Rochet ◽  
T Grémeaux ◽  
E Van Obberghen ◽  
Y Le Marchand-Brustel
Keyword(s):  
Protein Kinase C ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Obese Mice ◽  
Insulin Stimulation ◽  
Insulin Resistant ◽  
Kinase C ◽  
Dependent Component ◽  
Pkc Activation ◽  
Stimulation Of

The aim of our work was to investigate a possible role of protein kinase C (PKC) in insulin-stimulated glucose uptake in mouse skeletal muscle, and to search for a defect in PKC activation in insulin resistance found in obesity. In isolated soleus muscle of lean mice, insulin (100 nM) and 12-O-tetradecanoylphorbol 13-acetate (TPA) (1 microM) acutely stimulated glucose uptake 3- and 2-fold respectively. The effects of insulin and TPA were not additive. When PKC activity was down-regulated by long-term (24 h) TPA pretreatment, before measurement of glucose transport, the TPA effect was abolished, but in addition insulin-stimulated glucose transport returned to basal values. Furthermore, polymyxin B, which inhibits PKC in muscle extracts, prevented insulin-stimulated glucose uptake in muscle. In muscle of obese insulin-resistant mice, glucose uptake evoked by insulin was decreased, whereas the TPA effect, expressed as a fold increase, was unaltered. Thus both agents stimulated glucose transport to the same extent. Furthermore, no difference was observed when PKC activation by TPA was measured in muscle from lean and obese mice. These results suggest that: (1) PKC is involved in the insulin effect on glucose transport in muscle; (2) PKC activation explains only part of the insulin stimulation of glucose transport; (3) the defect in insulin response in obese mice does not appear to be due to an alteration in the PKC-dependent component of glucose transport. We propose that insulin stimulation of glucose uptake occurs by a sequential two-step mechanism, with first translocation of transporters to the plasma membrane, which is PKC dependent, and second, activation of the glucose transporters. In obesity only the activation step was decreased, whereas the translocation step was unaltered.

Assay of serum insulin and insulin-like activity on adipose tissue and muscle in vivo

Metabolism ◽  
1964 ◽  
Vol 13 (8) ◽  
pp. 769-774 ◽  
Author(s):  
George F. Cahill ◽  
Vilma Lauris ◽  
Stuart J. Soeldner ◽  
Dennis Slone ◽  
Jurgen Steinke
Keyword(s):  
Adipose Tissue ◽  
Serum Insulin ◽  
Insulin Like Activity

Stimulatory effects of cold exposure and cold acclimation on glucose uptake in rat peripheral tissues

1990 ◽  
Vol 259 (5) ◽  
pp. R1043-R1049 ◽  
Author(s):  
A. L. Vallerand ◽  
F. Perusse ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Peripheral Tissues ◽  
Brown Adipose ◽  
Shivering Thermogenesis ◽  
Stimulation Of

The effects of cold exposure on the net rates of 2-[3H]deoxy-D-glucose uptake (Ki) in rat peripheral tissues were investigated comparatively in warm- and cold-acclimated animals to determine whether cold acclimation induces regulatory alterations in glucose metabolism. Acute exposure of warm-acclimated (25 degrees C) rats to cold (48 h at 5 degrees C) markedly increased the Ki values in red and white skeletal muscles (2-5 times), in the heart (8 times), in several white adipose tissue (WAT) depots (4-20 times), and in brown adipose tissue (BAT) (110 times). After cold acclimation (3 wk at 5 degrees C), the Ki values further increased in the heart (15 times) and WAT (up to 29 times) but decreased in BAT (36 times). Remarkably, glucose uptake was still increased in muscles of cold-exposed/cold-acclimated animals (that do not shiver), demonstrating that enhanced glucose uptake may occur in muscles in the absence of shivering thermogenesis (or contractile activity). When cold-acclimated rats were returned to the warm for 18 h, the Ki values of all tissues, except WAT, returned to control levels. Cold exposure synergistically potentiated the stimulation of tissue glucose uptake induced by a maximal effective dose of insulin (0.5 U/kg iv) in warm- as well as in cold-acclimated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

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