Effect of Alloxan on Feed Consumption and on Replacement Therapy With Graded Levels of Insulin in Rats.

Kumaresan, Perianna; Turner, C. W.

doi:10.3181/00379727-122-31180

Cited by 8 publications

(3 citation statements)

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“…The pathogenesis of diabetic hyperphagia has been a focus of investigation since it was first documented experimentally more than 30 years ago (29), and many hypotheses have been forwarded to explain the phenomenon (30). Urinary loss of glucose, depletion of body fuel stores, and the inability to use glucose as an energy substrate were each proposed in early studies to explain the stimulatory effect of diabetes on food intake.…”

Section: Discussionmentioning

confidence: 99%

Low plasma leptin levels contribute to diabetic hyperphagia in rats.

et al. 1999

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The adipocyte hormone leptin reduces food intake in normal animals. During uncontrolled type 1 diabetes, plasma leptin levels fall, whereas food intake increases. To test the hypothesis that low leptin levels contribute to diabetic hyperphagia, we investigated the e ffect on food intake of replacement of leptin at basal plasma concentrations for 7 days in Long-Evans rats with uncontrolled diabetes induced by streptozotocin (STZ). One group of STZ diabetic rats received saline (STZ + Sal) (n = 11), while the other group (STZ + Lep) (n = 15) received a subcutaneous infusion of recombinant rat leptin (100 µg ؒ k g -1 ؒ d a y -1 ) via osmotic minipumps. A nondiabetic control group (Con) (n = 11) received saline only. In the STZ + Sal group, plasma leptin levels decreased by 75% (P < 0.05) from 2.4 ± 0.5 on the day before STZ/citrate buffer vehicle ( Veh) injection (day 0) to 0.6 ± 0.2 ng/ml on day 7. In contrast, plasma leptin levels on days 3-7 were comparable to pretreatment values in both the STZ + Lep group (day 0: 2.6 ± 0.4 vs. day 7: 2.5 ± 0.3 ng/ml, NS) and the Con group (day 0: 3.8 ± 0.4 vs. day 7: 2.9 ± 1.0 ng/ml, NS). In the STZ + Sal group, daily food intake increased gradually to values 43% above basal by day 7 (day 0: 24 ± 2 to day 7: 33 ± 3 g, P < 0.05), whereas food intake did not increase in either the STZ + Lep group (day 0: 24 ± 1 vs. day 7: 21 ± 2 g, NS), or the Con group (day 0: 23 ± 1 vs. day 7: 23 ± 2 g). Plasma glucose levels exceeded nondiabetic control values (7.7 ± 0.2 mmol/l) in both diabetic groups, but were lower in the STZ + Lep group (17.2 ± 1.8 mmol/l) than in the STZ + Sal group (24.3 ± 1.1 mmol/l, P < 0.05). To determine if sensitivity to leptin-induced anorexia was affected by STZ treatment, a second experiment was performed in which the effect of intracerebroventricular leptin injection (at doses of 0.35, 1.0, or 3.5 µg) on food intake was measured 10 days after STZ or Veh treatment. Leptin suppressed both 4-and 24-h food intake in the two groups to an equal extent at every dose (by 15, 22, and 35%, respectively). These findings support the hypothesis that the effect of uncontrolled diabetes to lower leptin levels contributes to diabetic hyperphagia and that this effect is not due to altered leptin sensitivity. T he hypothesis that body fat stores are subject to homeostatic regulation proposes that humoral signals generated in proportion to adiposity act in the central nervous system (CNS) to reduce food intake and body weight (1,2). Insulin, secreted from the pancreatic ␤-cells, and leptin (3), secreted from adipocytes, are both implicated in this homeostatic control system. Both hormones are secreted in proportion to body fat stores (4,5) and recent energy intake (6-8), and receptors for both insulin and leptin are concentrated in hypothalamic areas that control food intake and energy expenditure (9,10). Moreover, administration of either hormone into the brain (11-14) causes sustained reductions of food intake and body weight, whereas both insulin deficiency (as occurs in uncon...

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Section: Discussionmentioning

confidence: 99%

Low plasma leptin levels contribute to diabetic hyperphagia in rats.

et al. 1999

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“…Moreover, sympathetic outflow to thermogenic brown adipose tissue is reduced in both neuroglucopenia and uDM, and the reproductive, growth and thyroid axes are inhibited in both conditions as well. Therefore, in uDM, hyperglycaemia seems to be driven by many of the same behavioural, autonomic and neuroendocrine responses that are elicited by neuroglucopenia 9,132 .…”

Section: Emergency Circuits That Stimulate Feedingmentioning

confidence: 99%

Neurobiology of food intake in health and disease

2014

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Under normal conditions, food intake and energy expenditure are balanced by a homeostatic system that maintains stability of body fat content over time. However, this homeostatic system can be overridden by the activation of ‘emergency response circuits’ that mediate feeding responses to emergent or stressful stimuli. Inhibition of these circuits is therefore permissive for normal energy homeostasis to occur, and their chronic activation can cause profound, even life-threatening, changes in body fat mass. This Review highlights how the interplay between homeostatic and emergency feeding circuits influences the biologically defended level of body weight under physiological and pathophysiological conditions.

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“…Diabetic rats untreated with insulin may eat as much as 50% to 60% more food per day than their normal controls (13,14). In spite of this, the untreated diabetic liver donors lost weight or gained less than 15% of the weight gained by normal controls (15), and the insulin treated diabetic rats gained weight at about one half the normal rate.…”

Section: Animals and Induction Of Experimental Diabetes Mellitusmentioning

confidence: 99%

Effects of streptozotocin diabetes in the rat on blood levels of ten specific plasma proteins and on their net biosynthesis by the isolated perfused liver

et al. 1990

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Adult male Sprague-Dawley rats with streptozotocin-induced diabetes (6 to 8 wk duration), treated or untreated with insulin, were studied with two aims: (a) to ascertain whether protracted diabetes in the rat is associated with changes in circulating plasma protein levels analogous to those reported in human diabetic patients with clinical evidence of complications; (b) to evaluate the effects of experimental diabetes on the net cumulative biosynthesis of 10 specific plasma proteins by the isolated liver, perfused for 24 hr. Samples of liver donor plasma and samples of perfusate were analyzed by single radial immunodiffusion or by rocket immunoelectrophoresis for albumin, alpha 1-macroglobulin and the acute phase glycoproteins: fibrinogen, alpha 1-acid glycoprotein (Darcy), alpha 1-acid glycoprotein (Kawasaki), haptoglobin, alpha 2-(acute phase) globulin, hemopexin, C3-complement and ceruloplasmin. Diabetes (6 to 8 wk), untreated with insulin, resulted in significantly increased liver donor plasma levels of alpha 1-acid glycoprotein (Darcy) and alpha 1-acid glycoprotein (Kawasaki); plasma levels of hemopexin and of C3 decreased to 75% and 30% of normal, respectively. Insulin treatment of diabetic liver donors for 6 to 8 wk prevented the increase in alpha 1-acid glycoprotein (Darcy) and alpha 1-acid glycoprotein (Kawasaki) and minimized the decrease in C3 to 75% of normal. Perfused livers from untreated diabetic rats (6 to 8 wk) showed slightly decreased cumulative synthesis and secretion of alpha 1-acid glycoprotein (Darcy); however, synthesis of albumin was reduced to 35% of normal and that of eight glycoproteins ranged from 25% of normal (fibrinogen) to 12% of normal (C3). The striking in vitro induction of increased synthesis of acute-phase proteins by cortisol plus insulin in the isolated perfused normal liver was in contrast to the severely attenuated induction in perfused livers of untreated diabetic rats, which ranges from 50% of normal for alpha 1-acid glycoprotein (Darcy) to 5% of normal (C3). Severely negative perfusate nitrogen balance and impaired glucose utilization by perfused untreated diabetic livers contrasted with positive nitrogen balance and good glucose utilization of normal livers in response to insulin plus cortisol. The plasma protein synthetic capacity and the in vitro response to insulin plus cortisol of perfused livers from insulin-treated diabetic rats were normal for seven of the proteins but moderately decreased for albumin, haptoglobin and C3.

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Effect of Alloxan on Feed Consumption and on Replacement Therapy With Graded Levels of Insulin in Rats.

Cited by 8 publications

References 0 publications

Low plasma leptin levels contribute to diabetic hyperphagia in rats.

Low plasma leptin levels contribute to diabetic hyperphagia in rats.

Neurobiology of food intake in health and disease

Effects of streptozotocin diabetes in the rat on blood levels of ten specific plasma proteins and on their net biosynthesis by the isolated perfused liver

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