Resistance to diet-induced obesity: food intake, pancreatic sympathetic tone, and insulin

1987 ◽  
Vol 252 (3) ◽  
pp. R471-R478 ◽  
Author(s):  
B. E. Levin ◽  
J. Triscari ◽  
S. Hogan ◽  
A. C. Sullivan
Keyword(s):  
Weight Gain ◽  
Plasma Insulin ◽  
Caloric Intake ◽  
High Energy ◽  
Sympathetic Tone ◽  
Sprague Dawley ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Plasma Insulin Levels

After 15 wk on a moderately high-calorie high-fat (CM) diet, 43% of 40 3-mo-old male Sprague-Dawley rats developed diet-induced obesity (DIO) (29% more weight gain), whereas 57% of diet-resistant (DR) rats gained no more weight than 20 chow-fed controls. When switched to chow for another 7 wk, DR rats ate 13% less, gained 55% less weight, and had 49% lower food efficiency, whereas DIO rats ate 4% less but had comparable weight gain and efficiency to controls. DIO rats had 29% more carcass lipid (percent of carcass weight). DIO rat retroperitoneal white adipose pads had 65% more cells that were the same size as those in chow-fed pads; DR rat cells were similar to controls. Both DR and DIO rats increased norepinephrine turnover in their interscapular brown adipose pads by greater than 90%. DIO rats also had 40% lower pancreatic turnover; their plasma insulin levels were 327% of controls after 15 wk on the CM diet and 188% after 7 wk on chow. DR levels were the same as controls at both times. Therefore, regulation of caloric intake, pancreatic sympathetic tone, and plasma insulin levels were three important differences between rats that resisted and those that developed DIO on high-energy diets.

Diet cycling and age alter weight gain and insulin levels in rats

1994 ◽  
Vol 267 (2) ◽  
pp. R527-R535 ◽  
Author(s):  
B. E. Levin
Keyword(s):  
Weight Gain ◽  
Body Weight Gain ◽  
High Energy ◽  
Sprague Dawley ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Insulin Levels ◽  
Diet Intake

For assessment of the effect of diet cycling on body weight gain patterns, 3-mo-old male Sprague-Dawley rats were either cycled from chow to a high-energy condensed milk (CM) diet, back to chow, and then back to CM diet at 3-mo intervals (cyclers) or were fed chow to 9 mo of age and then CM diet for 3 mo (noncyclers). Nine of 21 cyclers developed diet-induced obesity (DIO), gaining 36, 59, and 281% more weight than chow-fed controls (CF) at each cycle, respectively. Twelve cycled rats were diet-resistant (DR) with comparable weight gain to CF rats after the first CM diet and chow cycles. However, they gained 202% more than CF rats and 50% more, with 29% heavier retroperitoneal fat pads, than noncycled DR rats after their second CM diet cycle begun at 9 mo of age. Enhanced weight gain in DR cyclers was probably due to enhanced food efficiency in the last few weeks of CM diet intake. Plasma insulin levels were 70% higher in cycled vs. noncycled DIO and DR rats, and both were higher than CF rats. Unlike 6-mo-old DR rats in a prior study, 12-mo-old noncycled DR rats after 3 mo on CM diet here had 45-172% higher alpha 2-adrenoceptors binding in 6 of 17 brain areas than noncycled DIO and/or CF rats. Thus age, diet cycling, and brain alpha 2-adrenoceptors interact to affect long-term changes in weight gain and metabolism.

Brown adipose and metabolic features of chronic diet-induced obesity

1985 ◽  
Vol 248 (6) ◽  
pp. R717-R723 ◽  
Author(s):  
B. E. Levin ◽  
M. Finnegan ◽  
J. Triscari ◽  
A. C. Sullivan
Keyword(s):  
Metabolic Efficiency ◽  
Sprague Dawley ◽  
High Fat ◽  
Interscapular Brown Adipose Tissue ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Norepinephrine Turnover ◽  
Brown Adipose ◽  
Plasma Insulin Levels

Half of the 3-mo male Sprague-Dawley rats fed a high-fat (DIO) diet for 5 mo became obese and had increased carcass lipid (106%) and plasma insulin levels (61%), despite 8% less total energy intake than chow-fed controls. Their interscapular brown adipose tissue (IBAT) was 52% heavier with 45% more lipid and larger uni- and multilocular cells. Norepinephrine turnover was normal in their hearts, pancreases, and aortas but undetectable in IBAT where in vitro lipolysis, but not O2 consumption (VO2), was enhanced. Half the rats fed the DIO diet ate 17% fewer calories, gained weight equally to controls, but still had 34% more carcass lipid. Their IBAT was heavier, contained 103% more protein, with no detectable norepinephrine turnover, whereas maximal lipolysis was 73% lower and maximal VO2 was the same or even lower than controls. IBAT VO2 was stimulated by switching 8-mo chow-fed controls to the DIO diet for 7 days (which caused a 480% greater weight gain) but not by switching 8-mo obese rats to chow for 3 days. Therefore metabolic efficiency was increased while BAT VO2 and norepinephrine turnover were unchanged or reduced compared with controls by either chronic obesity or a high-fat diet.

Ontogeny of diet-induced obesity in selectively bred Sprague-Dawley rats

2003 ◽  
Vol 285 (3) ◽  
pp. R610-R618 ◽  
Author(s):  
Matthew R. Ricci ◽  
Barry E. Levin
Keyword(s):  
Leptin Receptor ◽  
Splice Variants ◽  
Caloric Intake ◽  
High Energy ◽  
Sprague Dawley ◽  
Low Fat Diet ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Outbred Sprague-Dawley rats selectively bred for their propensity to develop diet-induced obesity (DIO) become heavier on low-fat diet than those bred to be diet resistant (DR) beginning at ∼5 wk of age. Here we assessed the development of metabolic and neural functions for insights into the origins of their greater weight gain. From week 5 to week 10, chow-fed DIO rats gained 15% more body weight and ate ∼14% more calories but had only slightly greater adiposity and plasma leptin than DR rats. From day 3 through week 10, DIO and DR rats had similar mRNA expression of arcuate nucleus neuropeptide Y, proopiomelanocortin, agouti-related peptide, and all splice variants of the leptin receptor (OB-R). When fed a high-energy (HE; 31% fat) diet, 7-wk-old DIO rats had a 240% increase in plasma leptin levels after only 3 days. Despite this early leptin rise, they maintained a persistent hyperphagia and became more obese than chow-fed DIO rats and DR rats fed chow or HE diet. Their failure to reduce caloric intake, despite high levels of leptin, suggests that selectively bred DIO rats might have reduced leptin sensitivity similar to that seen in the outbred DIO parent strain.

Glucose-induced norepinephrine levels and obesity resistance

1987 ◽  
Vol 253 (3) ◽  
pp. R475-R481 ◽  
Author(s):  
B. E. Levin ◽  
A. C. Sullivan
Keyword(s):  
Weight Gain ◽  
Caloric Intake ◽  
Sympathetic Activation ◽  
Glucose Load ◽  
Sprague Dawley ◽  
Intravenous Glucose ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Calorie Diet ◽  
High Calorie

The value of glucose-stimulated sympathetic activation in differentiating rats that would subsequently resist or develop diet-induced obesity (DIO) when chronically fed a high-calorie diet (CM) enriched in fat and sucrose was tested in 3-mo-old male Sprague-Dawley rats. While the rats were on chow the areas under the curve for plasma glucose, insulin, and norepinephrine (NE) levels were measured for 60 min after an intravenous glucose load (1 g/kg). Half of the rats then switched to the CM diet for 14 wk developed DIO with 54% more weight gain and 205% heavier retroperitoneal fat pads; half [diet resistant (DR)] had weight gain and pad weights comparable to chow-fed controls. Caloric intake was comparable in all animals. NE areas after intravenous glucose loads were 54% lower in DR than DIO rats, and there was a positive correlation (r = 0.63) between these NE areas and subsequent weight gain on the CM diet. Areas under the insulin curve correlated with subsequent weight gain on chow (r = 0.71) but not the CM diet. These results suggest that rats predisposed to become DR on the CM diet have dampened sympathetic activation after a glucose load, possibly because of heightened end-organ responsiveness to NE.

scholarly journals Down-regulation of β3-adrenergic receptor expression in rat adipose tissue during the fasted/fed transition: evidence for a role of insulin

1997 ◽  
Vol 323 (2) ◽  
pp. 359-364 ◽  
Author(s):  
Khadija El HADRI ◽  
Christine CHARON ◽  
Jacques PAIRAULT ◽  
Sylvie HAUGUEL-DE MOUZON ◽  
Annie QUIGNARD-BOULANGÉ ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adrenergic Receptor ◽  
Plasma Insulin ◽  
Present Report ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Insulin Levels ◽  
Brown Adipose ◽  
Plasma Insulin Levels ◽  
Rat Adipose Tissue

The β3-adrenergic receptor (β3-AR) exerts a central role in the transduction of catecholamine effects in white and brown adipose tissue (WAT and BAT). A recent report has documented that insulin strongly down-regulates β3-AR expression and catecholamine responsiveness in 3T3-F442A adipocytes [Fève, El Hadri, Quignard-Boulangé and Pairault (1994) Proc. Natl. Acad. Sci. U.S.A. 91, 5677–5681]. In the present report we show that the rise in plasma insulin levels elicited by the fasted/fed transition is associated with a reduction in β3-AR mRNA levels and β-adrenergic responsiveness in WAT and BAT. β3-AR transcripts are also decreased in adipose tissue from animals subjected for 6 h to euglycaemic hyperinsulinaemic glucose clamps. Moreover, insulin acts directly on cultured rat white and brown adipocytes to decrease β3-AR gene expression and adenylate cyclase activity in response to β3-AR-selective agonists. These results suggest that there is a close relationship between food intake, plasma insulin levels and β3-AR expression.

scholarly journals Lower plasma insulin levels during overnight closed-loop in school children with type 1 diabetes: Potential advantage? A randomized cross-over trial

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0212013 ◽  
Author(s):  
Ulrike Schierloh ◽  
Malgorzata E. Wilinska ◽  
Ineke M. Pit-ten Cate ◽  
Petra Baumann ◽  
Roman Hovorka ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
School Children ◽  
Plasma Insulin ◽  
Closed Loop ◽  
Lower Plasma ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Insulin ◽  
Metformin Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

Defense of differfing body weight set points in diet-induced obese and resistant rats

1998 ◽  
Vol 274 (2) ◽  
pp. R412-R419 ◽  
Author(s):  
Barry E. Levin ◽  
Richard E. Keesey
Keyword(s):  
Body Weight ◽  
Diet Composition ◽  
Energy Homeostasis ◽  
Energy Content ◽  
Sprague Dawley ◽  
Fat Pad ◽  
Insulin Levels ◽  
Diet Induced Obesity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Among outbred Sprague-Dawley rats, approximately one-half develop diet-induced obesity (DIO) and one-half are diet resistant (DR) on a diet relatively high in fat and energy content (HE diet). Here we examined the defense of body weight in these two phenotypes. After HE diet for 13 wk, followed by chow for 6 wk, DR rats gained weight comparably but their plasma leptin levels fell to 54% of chow-fed controls. When a palatable liquid diet (Ensure) was added for 13 wk, other DR rats became obese. But when switched to chow, their intakes fell by 60%, and body and retroperitoneal (RP) fat pad weights and plasma leptin and insulin levels all declined for 2 wk and then stabilized at control levels after 6 wk. In contrast, comparably obese DIO rats decreased their intake by only 20%, and their weights plateaued when they were switched to chow after 13 wk on HE diet. When a subgroup of these DIO rats was restricted to 60% of prior intake, their weights fell to chow-fed control levels over 2 wk. But their leptin and insulin levels both fell disproportionately to 30% of controls. When no longer restricted, their intake and feed efficiency rose immediately, and their body and RP pad weights and leptin and insulin levels rose to those of unrestricted DIO rats within 2 wk. Thus diet and genetic background interact to establish high (DIO) or low (DR) body weight set points, which are then defended against subsequent changes in diet composition and/or energy availability. If leptin affects energy homeostasis, it does so differentially in DIO vs. DR rats since comparably low and high levels were associated with differing patterns of weight change between the two phenotypes.

scholarly journals Brown adipose tissue activity is modulated in olanzapine-treated young rats by simvastatin

2020 ◽  
Author(s):  
Xuemei Liu ◽  
Xiyu Feng ◽  
Chao Deng ◽  
Lu Liu ◽  
Yanping Zeng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
Peroxisome Proliferator ◽  
Sprague Dawley ◽  
Olanzapine Treatment ◽  
Brown Adipose

Abstract BackgroundPrescription of second-generation antipsychotic drugs (SGAs) to childhood/adolescent has exponentially increased in recent years, which was associated with the greater risk of significant sedation, weight gain, and dyslipidemia. Statin is considered a potential preventive and treatment approach for reducing SGA-induced weight gain and dyslipidemia in schizophrenia patients. However, the effect of statin treatment in children and adolescents with SGA-induced dyslipidemia is not clearly demonstrated.MethodsTo investigate the efficacy of interventions of statin aimed at reversing SGA-induced dyslipidemia, young Sprague Dawley (SD) rats were treated orally with either olanzapine (1.0 mg/kg, t.i.d.), simvastatin (3.0 mg/kg, t.i.d.), olanzapine plus simvastatin (O+S), or vehicle (control) for 5 weeks.ResultsOlanzapine treatment increased weight gain, food intake and feeding efficiency compared to the control, while O+S co-treatment significantly reversed body weight gain but had no significant effect on food intake. Moreover, olanzapine treatment induced a slight but significant reduction in body temperature, with a decrease in locomotor activity. Fasting plasma glucose, triglycerides (TG), and total cholesterol (TC) levels were markedly elevated in the olanzapine-only group, whereas O+S co-treatment significantly ameliorated these changes. A down-regulating of uncoupling protein-1 (UCP1) and peroxisome-proliferator-activated receptor-γ co-activator-1α (PGC-1α) expression was observed in brown adipose tissue (BAT) in the olanzapine-only group, following a significant decrease in the ratio of phosphorylated PKA (p-PKA)/PKA. Interestingly, these protein changes could be reversed by co-treatment with O+B. Our results demonstrated simvastatin to be effective in ameliorating TC and TG elevated by olanzapine.ConclusionsModulation of BAT activity could be a partial mechanism in reducing metabolic side effects caused by SGAs in child and adolescent patients.

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