Enhanced thermogenesis during recovery from diet-induced weight gain in the rat

Abstract

The present study examined the contribution of energy expenditure to the recovery of body weight after a period of overfeeding. Three groups of 2-mo-old female rats (n = 24) were fed, respectively, a 10% (wt/wt)-fat diet (control), a 35% (wt/wt)-fat diet (high fat) or were force fed 130% of the control diet (tube fed). After 30 days, all groups received the control diet for 18 days of recovery. Both overfeeding protocols significantly increased weight above control levels. This difference disappeared after 7 days of recovery. Increases in resting oxygen consumption, serum 3,5,3'-triiodothyronine (T3) levels, and the thermogenic response to norepinephrine were observed at the end of overfeeding. Serum T3 and resting oxygen consumption returned to control levels by day 3 of recovery from overfeeding, whereas the thermogenic response to norepinephrine required 9 days to recover. Whereas total energy expenditure was not significantly elevated during overfeeding, significant increases of 9.6 and 13.9% were observed in the formerly high-fat and tube-fed animals, respectively, during recovery. These data indicate that changes in energy expenditure play an important role in maintaining the stability of body weight.

Maintenance of the thyroid axis during diet-induced obesity in rodents is controlled at the central level

“…Previous studies have shown that thyroid hormone levels increase during DIO (1,30). Consistent with these early findings, the current report demonstrates that in DIO rats there is an increase in thyroid hormones as well as an increase in prepro-TRH mRNA, TRH, and pSTAT3 signaling in TRH neurons.…”

Adaptive thermogenesis and uncoupling proteins: a reappraisal of their roles in fat metabolism and energy balance

“…This postoverfeeding sustained elevation of thermogenesis, also observed in laboratory rats [110,111], is consistent with a feedback mechanism existing between thermogenesis and body fat-i.e., the result of an activated adipose-specific control of thermogenesis, which may well have contributed to the subsequent slow return of body weight towards the baseline level after the phase of fat overshooting.…”

Impacts of Embryonic Thermal Programming on the Expression of Genes Involved in Foie gras Production in Mule Ducks

“…Although no impact of thermal programming could be measured on plasma T3 and T4 levels in our overfed ducks ( Massimino et al, 2019 ), increased expression of this deiodinase in the TM group suggests that embryonic thermal programming may induce a slight TH inactivation in the liver. These data support the hypothesis that embryonic thermal manipulation could have increased the lipid content in the liver by decreasing energy expenditure via thermogenesis ( Almeida et al, 1996 ). Even though we did not measure a difference in surface temperature after the OF period in our programmed ducks, it is not impossible that internal temperature and thus thermogenesis was affected, reducing energy expenditure and thus promoting liver fattening.…”

“…Our expression data seem to confirm a global activation of T3 in the liver of overfed ducks, since we measured an increase in THRB and SPOT14 (involved in T3-induced lipid synthesis) expressions, in parallel with a decrease in NCOR (corepressor) and DIO3 (deiodinase responsible for TH inactivation) ( Kinlaw et al, 1995 ; Mendoza and Hollenberg, 2017 ; Sinha et al, 2018 ; Ritter et al, 2020 ). This increase in T3 activity during overfeeding has been proposed as a protective mechanism to limit weight gain by increasing lipid catabolism in favor of energy expenditure through thermogenesis ( Oppenheimer et al, 1991 ; Almeida et al, 1996 ; Silvestri et al, 2005 ). These regulations therefore suggest a protective mechanism for liver cells to limit OF-induced lipid overload, which may alter cell physiology over time.…”