The effects of sympathectomy and dexamethasone in rats ingesting sucrose

Abstract

Both high-sucrose diet and dexamethasone (D) treatment increase plasma insulin and glucose levels and induce insulin resistance. We showed in a previous work (Franco-Colin, et al. Metabolism 2000; 49:1289-1294) that combining both protocols for 7 weeks induced less body weight gain in treated rats without affecting mean daily food intake. Since such an effect may be explained by an increase in caloric expenditure, possibly due to activation of the sympathetic nervous system by sucrose ingestion, in this work, and using 10% sucrose in the drinking water, male Wistar rats were divided into 4 groups. Two groups were sympathectomized using guanethidine (Gu) treatment for 3 weeks. One of these groups of rats received D in the drinking water. Of the 2 groups not receiving Gu, one was the control (C) and the other received D. After 8 weeks a glucose tolerance test was done. The rats were sacrificed and liver triglyceride (TG), perifemoral muscle lipid, and norepinephrine (NE) levels in the liver spleen, pancreas, and heart were determined. Gu-treated rats (Gu and Gu+D groups) showed less than 10% NE concentration compared to C and D rats, less daily caloric intake and body-weight gain, more sucrose intake, and better glucose tolerance. The area under the curve after glucose administration correlated significantly with the mean body weight gain of the rats, except for D group. Groups D (D and Gu+D) also showed less caloric intake and body-weight gain but higher liver weight and TG concentration and lower peripheral muscle mass. The combination of Gu+D treatments showed some peculiar results: negative body weight gain, a fatty liver, and low muscle mass. Though the glucose tolerance test had the worst results for the D group, it showed the best results in the Gu+D group. There were significant interactions for Guan X Dex by twoway ANOVA test for the area under the curve in the glucose tolerance test, muscle mass, and muscle lipids. The results suggest that dexamethasone catabolic effect is not caused by sympathetic activation.

Biochemical and morphological attributes of broiler kidney in response to dietary glucocorticoid, dexamethasone

“…At day 28, significantly increased number of atrophied glomerulus was seen along with collapse of tubular structure. These findings are in agreement with Franco-Colín et al, 2006 , Salman and Hassooni, 2020 . There was also extensive inflammation and fibrosis despite the serum HDL significantly increased from day 21.…”

Low‐Dose Dexamethasone Treatment Promotes the Pro‐Survival Signalling Pathway in the Adult Rat Prefrontal Cortex

“…It is well established that the low-dose subchronic DEX treatment strongly exerts peripheral actions, causing profound suppression of the HPA axis, atrophy of the adrenal glands (2), thymic involution in rodents through apoptosis (28) and a decrease of body weight via the disturbance of lipid (29) and glucose metabolism (30). Hence, in our model system, hormone treatment efficacy is confirmed by a severe body weight loss and a dramatic reduction of thymus and adrenal gland weight, as well by a significant decrease of CORT levels in the serum.…”

Dissection of glucocorticoid receptor-mediated inhibition of the hypothalamic–pituitary–adrenal axis by gene targeting in mice

“…This ramification is supported by rat studies showing that prenatal dexamethasone application causes low birth weight (Drake et al, 2010), but dexamethasone application into adult rats causes an increase in enzymes responsible for synthesis of lipids, and thus increased visceral adiposity (Chimin et al, 2014). However evidence in most studies demonstrates catabolic effects of dexamethasone in adult rodents that lead to weight loss (Franco-Colín et al, 2006; Minet-Quinard et al, n.d.; Savary et al, 1998). Thus the cause of discordance in weight between adult Sim1Cre-GRe3Δ and GR flox/+ ;Sim1Cre + mice is unclear, given that excess GCs also occurs in these lines.…”