Lipolytic responsiveness to epinephrine in nondiabetic and diabetic humans

1997 ◽  
Vol 272 (6) ◽  
pp. E1130-E1135 ◽  
Author(s):  
G. D. Divertie ◽  
M. D. Jensen ◽  
P. E. Cryer ◽  
J. M. Miles
Keyword(s):  
Adipose Tissue ◽  
Insulin Dependent Diabetes ◽  
Response Curves ◽  
Epinephrine Infusion ◽  
Hormone Levels ◽  
Control Subjects ◽  
Insulin Dependent ◽  
Adipose Tissue Lipolysis ◽  
Plasma Hormone ◽  
Beta Hydroxybutyrate

To determine whether the sensitivity of adipose tissue lipolysis to catecholamines is increased in poorly controlled insulin-dependent diabetes, the lipolytic response to epinephrine was measured in seven nondiabetic volunteers and seven poorly controlled diabetic subjects with use of [1-(14)C]palmitate as a tracer. Subjects received sequential 1-h infusions of epinephrine, which produced epinephrine concentrations of approximately 1,000, approximately 1,750, approximately 3,500, and approximately 6,000 pmol/l. A pancreatic clamp was used to maintain constant plasma hormone levels. Concentration-response curves were constructed for each subject from the integrated lipolytic response during each epinephrine infusion. There was no difference in maximal lipolytic response (117 +/- 19 vs. 152 +/- 11 mumol.kg-1.h-1) or in maximally effective (3,171 +/- 267 vs. 3,357 +/- 349 pmol/l) or half-maximally effective (1,081 +/- 109 vs. 1,015 +/- 120 pmol/l) epinephrine concentrations between nondiabetic and diabetic subjects, respectively (all P = NS). In control subjects, maximum beta-hydroxybutyrate concentrations were achieved at lower epinephrine concentrations than those required for a maximum lipolytic effect. Thus, under pancreatic clamp conditions, the lipolytic response to epinephrine in nondiabetic and diabetic subjects was similar.

Effect of Posture and Acute Glycaemic Control on the Excretion of Retinol-Binding Protein in Normoalbuminuric Insulin-Dependent Diabetic Patients

1993 ◽  
Vol 84 (4) ◽  
pp. 461-467 ◽  
Author(s):  
Carlo Catalano ◽  
Peter H. Winocour ◽  
Susan Gillespie ◽  
Ian Gibb ◽  
K. George M. M. Alberti
Keyword(s):  
Blood Glucose Concentration ◽  
Excretion Rate ◽  
Binding Protein ◽  
Insulin Dependent Diabetes ◽  
Retinol Binding Protein ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Protein Excretion ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

1. It has been suggested that tubular damage may precede gomerular damage at the onset of diabetic nephropathy. This may be reflected by increased urinary excretion of low-molecular-mass proteins, such as retinol-binding protein. 2. We have measured the urinary excretion rate of retinol-binding protein overnight, during orthostasis and during a hyperinsulinaemic euglycaemic clamp (blood glucose concentration 7.0 mmol/l) with stable diuresis in 34 normotensive, normoalbuminuric insulin-dependent diabetic patients and in 10 normal control subjects. Normal control subjects were not clamped. A further four normoalbuminuric insulin-dependent diabetic patients were rendered euglycaemic without a water load. 3. Overnight retinol-binding protein excretion rate was 58 (16-157) [median(range)] ng/min in patients with insulin-dependent diabetes and 32 (15-72) ng/min in control subjects (P < 0.01). The excretion rate did not change during orthostasis [patients with insulin-dependent diabetes, 67 (3-173) ng/min; control subjects, 23 (5-78) ng/min]. During the euglycaemic clamp retinol-binding protein excretion rate increased to 383 (78-4897) ng/min in patients with insulin-dependent diabetes (P < 0.01). An average increment in retinol-binding protein excretion rate of greater than 4000% was noted after acute euglycaemia in those patients with insulin-dependent diabetes who were not water-loaded. 4. In insulin-dependent diabetes, both overnight and orthostatic retinal-binding protein excretion was not correlated with fasting blood glucose concentration, HbA1, fructosamine or duration of diabetes. The absolute and incremental excretion rates of retinol-binding protein during the clamp were, however, correlated with both fasting blood glucose concentration and glucose excretion rate (rs = 0.41-0.48, P < 0.01). 5. The study demonstrates that retinol-binding protein excretion is increased in insulin-dependent diabetes in the absence of microalbuminuria and that this increase in retinol-binding protein excretion is particularly pronounced after acute euglycaemia. Acute tubular dysfunction related to acute changes in glucose control appears to be the most likely explanation, but established tubular damage could also be implicated. Postural variation in retinol-binding protein excretion was not detected.

scholarly journals Changes in the sensitivity to glucagon of lipolysis in adipocytes from pregnant and lactating rats

1988 ◽  
Vol 254 (3) ◽  
pp. 661-665 ◽  
Author(s):  
V A Zammit
Keyword(s):  
Adipose Tissue ◽  
The Other ◽  
High Concentration ◽  
Response Curves ◽  
Pregnant Rats ◽  
Adipose Tissue Lipolysis ◽  
The Right ◽  
Peak Lactation ◽  
Stimulation Of

1. Rates of lipolysis were measured at different concentrations of glucagon in adipocytes prepared from parametrial adipose tissue of fed or starved rats in different reproductive states. All experiments were performed in the presence of a high concentration of adenosine deaminase (1 unit/ml). 2. Maximal rates of lipolysis (elicited by 25 nM-glucagon in each instance) were higher in adipocytes from peak-lactating rats than those from pregnant animals in both the fed and starved states. 3. Of adipocytes from fed animals, those from peak-lactating rats were the most sensitive to glucagon, whereas those from late-pregnant and early-lactating rats were 1-2 orders of magnitude less sensitive. 4. Adipocytes from 24 h-starved rats showed a much smaller stimulation of lipolysis by glucagon, making the assessment of sensitivity difficult. Therefore, rates of lipolysis were also measured in the presence of a maximally anti-lipolytic dose of insulin. The presence of insulin did not alter the relative sensitivities to glucagon of adipocytes from fed animals in different reproductive states, although all dose-response curves were shifted to the right. When lipolysis in adipocytes from starved animals was measured in the presence of insulin, it became evident that starvation for 24 h markedly increased the sensitivity of adipocytes from late-pregnant rats to glucagon, but did not affect that of cells from animals in the other reproductive states. 5. It is concluded that the large changes in sensitivity to glucagon that occurred during the reproductive cycle may enable the modulation of adipose-tissue lipolysis in vivo to satisfy the different metabolic requirements of the animal in the transition from pregnancy to peak lactation.

Increased Concentrations of Total IgM At Clinical Onset of Type 1 (Insulin-Dependent) Diabetes: Correlation with IgM Binding to Cells. The Belgian Diabetes Registry

1992 ◽  
Vol 38 (9) ◽  
pp. 1762-1767 ◽  
Author(s):  
T Decraene ◽  
C Vandewalle ◽  
D Pipeleers ◽  
F K Gorus
Keyword(s):  
Matched Control ◽  
Islet Cells ◽  
Insulin Dependent Diabetes ◽  
Diabetes Registry ◽  
Control Subjects ◽  
Clinical Onset ◽  
Natural Autoantibodies ◽  
Insulin Dependent ◽  
Age And Sex

Abstract Eighty patients with type 1 (insulin-dependent) diabetes (ages 0-39 years) were consecutively recruited by the Belgian Diabetes Registry. Sera obtained at clinically diagnosed onset (i.e., before start of insulin therapy or within 7 days of initial treatment) were analyzed for total IgM concentrations and for IgM binding to fixed rat splenocytes (IgM-LyAb) and permeabilized rat islet cells (IgM-ICAb). Comparison of results with those in age- and sex-matched control subjects, by fluorescence-activated cell-sorter analysis, indicated greater concentrations of IgM-LyAb and IgM-ICAb in sera from the patients. IgM antibodies reacted indiscriminately with islet beta and islet endocrine non-beta cells. The prevalence of IgM-ICAb, but not of IgM-LyAB, was significantly (P less than 0.05) higher in patients than in the control subjects. Of the ICAb-positive patients, 54% were also LyAb-positive, whereas none of the control subjects were doubly positive. IgM-ICAb and IgM-LyAb binding signals were positively correlated. Serum IgM concentrations were significantly (P less than 0.001) greater in patients than in control subjects and were significantly correlated with IgM-LyAb (P less than 0.001) and IgM-ICAb (P less than 0.01). The positivity for IgM binding was not, however, merely a reflection of total IgM, because no such correlation was found in sera from seven patients with Waldenström macroglobulinemia. Clinical onset of type 1 diabetes is apparently accompanied by increased production of IgM. The correlation between IgM concentrations and IgM binding to islet cells might reflect polyclonal activation or natural autoantibodies.

Impaired Endothelium-Dependent and Independent Dilatation of Forearm Resistance Arteries in Men with Diet-Treated Non-Insulin-Dependent Diabetes: Role of Dyslipidaemia

1996 ◽  
Vol 91 (5) ◽  
pp. 567-573 ◽  
Author(s):  
G. F. Watts ◽  
S. F. O'brien ◽  
W. Silvester ◽  
J. A. Millar
Keyword(s):  
Sodium Nitroprusside ◽  
Density Lipoprotein ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
Diabetic Patients ◽  
Resistance Arteries ◽  
Control Subjects ◽  
Vasodilatory Response ◽  
Insulin Dependent

1. We measured endothelium-dependent and independent dilatation of forearm resistance arteries in 29 men with diet-treated non-insulin-dependent diabetes mellitus and 18 age- and sex-matched control subjects. None of the diabetic patients had hypercholesterolaemia, overt hypertension or microproteinuria. 2. We examined endogenous and exogenous nitric oxide-mediated vasodilatation by measuring forearm blood flow with venous occlusive plethysmography after administration of acetylcholine (7.5 and 15 μg/min) and sodium nitroprusside (3 and 10 μg/min), respectively, into the brachial artery. NG-monomethyl-l-arginine was also infused to study the inhibition of basal and stimulated release of nitric oxide. 3. The vasodilatory response to acetylcholine, expressed as area under curve, was significantly decreased in the diabetic patients compared with the control subjects (P = 0.019). NG-monomethyl-l-arginine significantly reduced basal (P < 0.001) and acetylcholine-stimulated blood flow (P < 0.02) in both groups. The vasodilatory response (also expressed as area under curve) to sodium nitroprusside was significantly less (P = 0.044) in the diabetic patients than in the control subjects. 4. In the diabetic patients, impaired vasodilatory responses to acetylcholine were significantly correlated with higher serum triacylglycerols (P = 0.048) and lower high-density lipoprotein-cholesterol concentrations (P = 0.007); the association with high-density lipoprotein was independent of age, glycated haemoglobin and blood pressure. Sodium nitroprusside responses were not correlated with lipid and lipoprotein concentrations. 5. We conclude that there is impaired endothelial and smooth muscle cell function in men with diet-treated non-insulin-dependent diabetes mellitus uncomplicated by overt hypertension or microproteinuria. Endothelial dysfunction may be related to diabetic dyslipidaemia and associated metabolic disturbances.

scholarly journals Efficacy and Safety of Allogenic Canine Adipose Tissue-derived Mesenchymal Stem Cell Therapy for Insulin Dependent Diabetes Mellitus in Dogs: A pilot study

2019 ◽  
Author(s):  
Sung-Yong Rhew ◽  
Woo-Jin Song ◽  
Qiang Li ◽  
Ju-Hyun An ◽  
Hyung-Kyu Chae ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Stem Cell ◽  
Pilot Study ◽  
Diabetic Complications ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Dependent Diabetes ◽  
Dependent Diabetes Mellitus ◽  
C Peptide ◽  
Insulin Dependent

Abstract Background Since mesenchymal stem cells (MSCs) possess regenerative and immunomodulatory properties, and are capable of controlling the immune dysregulation that leads to β-cell destruction, stem cell transplantation could be used in the management of insulin-dependent diabetes mellitus (IDDM). In this pilot study, we assessed whether canine adipose tissue-derived MSC (cAT-MSC) therapy could be an option for treatment of canine diabetes mellitus. Results With the written informed consent of the owners, allogenic cAT-MSCs were infused intravenously in IDDM dogs. C-peptide was elevated by about 5–15% in 3 of 4 cases, and hyperlipidemia was resolved in 2 of 4 cases. Additionally, fructosamine and Hb/A1c levels were improved in 2 of 4 cases. Conclusions Considering that C-peptide secretion capacity and lipid metabolism are related to diabetic complications, these results suggest that cAT-MSC therapy in diabetic dogs might help to improve the insulin secretory capacity of dogs with IDDM and prevent diabetic complications.

Lack of effect of hyperglycemia on lipolysis in humans

1993 ◽  
Vol 265 (6) ◽  
pp. E821-E824 ◽  
Author(s):  
E. Cersosimo ◽  
S. Coppack ◽  
M. Jensen
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Glucose ◽  
Acid Metabolism ◽  
The Face ◽  
Study Interval ◽  
Free Fatty Acid Metabolism ◽  
Insulin Dependent ◽  
Adipose Tissue Lipolysis

To examine whether hyperglycemia is an independent regulator of adipose tissue lipolysis, we measured palmitate flux ([3H]palmitate) on two occasions in eight volunteers with insulin-dependent diabetes. On one. occasion, euglycemia was maintained for 4 h continuously; on a different occasion, hyperglycemia (plasma glucose, 12 mmol/l) was induced after 2 h of euglycemia. Palmitate flux decreased from 1.39 +/- 0.22 to 1.25 +/- 0.18 mumol.kg-1 x min-1 during sustained euglycemia and from 1.43 +/- 0.24 to 1.13 +/- 0.19 mumol.kg-1 x min-1 during the transition from the euglycemic to the hyperglycemic study intervals. There were no significant differences between the changes in palmitate flux from the first to the second study interval on the control (euglycemia-euglycemia) and experimental (euglycemia-hyperglycemia) study days and no difference between palmitate flux on different study days. Thus, in the face of euinsulinemia, euglucagonemia, and the absence of somatostatin, no effect of hyperglycemia on free fatty acid metabolism could be detected in humans.

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