A Role for Adipose Tissue De Novo Lipogenesis in Glucose Homeostasis During Catch-up Growth

Marcelino, Helena; Veyrat-Durebex, Christelle; Summermatter, Serge; Sarafian, Delphine; Miles-Chan, Jennifer L.; Arsenijevic, Denis; Zani, Fabio; Montani, Jean‐Pierre; Seydoux, Josiane; Solinas, Giovanni; Rohner‐Jeanrenaud, Françoise; Dulloo, Abdul G.

doi:10.2337/db12-0255

Cited by 48 publications

(55 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This evidence supports the hypothesis that early catch-up fat of the H1N offspring is not associated with overt adipocyte hypertrophy or inflammation. 68 These results suggested that a preweaning H1N diet programmed the pathophysiological changes of adipose tissue at least partially through the upregulation of genes involved in adipogenesis and lipogenesis.…”

Section: Discussionmentioning

confidence: 87%

A short-term transition from a high-fat diet to a normal-fat diet before pregnancy exacerbates female mouse offspring obesity

Olson

Rasmussen

et al. 2015

Int J Obes

View full text Add to dashboard Cite

BACKGROUND/OBJECTIVES Recent findings have highlighted the detrimental influence of maternal overnutrition and obesity on fetal development and early life development. However, there are no evidence-based guidelines regarding the optimal strategy for dietary intervention before pregnancy. SUBJECTS/METHODS We used a murine model to study whether switching from a high-fat (HF) diet to a normal-fat (NF) diet (H1N group) 1 week before pregnancy could lead to in utero reprogramming of female offspring obesity; comparator groups were offspring given a consistent maternal HF group or NF group until weaning. After weaning, all female offspring were given the HF diet for either 9 or 12 weeks before being killed humanely. RESULTS H1N treatment did not result in maternal weight loss before pregnancy. NF offsprings were neither obese nor glucose intolerant during the entire experimental period. H1N offsprings were most obese after the 12-week postweaning HF diet and displayed glucose intolerance earlier than HF offsprings. Our mechanistic study showed reduced adipocyte insulin receptor substrate 1 (IRS1) and hepatic IRS2 expression and increased adipocyte p-Ser636/639 and p-Ser612 of H1N or HF offspring compared with that in the NF offspring. Among all groups, the H1N offspring had lowest level of IRS1 and the highest levels of p-Ser636/639 and p-Ser612 in gonadal adipocyte. In addition, the H1N offspring further reduced the expression of Glut4 and Glut2, vs those of the HF offspring, which was lower compared with the NF offspring. There were also enhanced expression of genes inhibiting glycogenesis and decreased hepatic glycogen in H1N vs HF or NF offspring. Furthermore, we showed extremely higher expression of lipogenesis and adipogenesis genes in gonadal adipocytes of H1N offspring compared with all other groups. CONCLUSIONS Our results suggest that a transition from an HF diet to an NF diet shortly before pregnancy, without resulting in maternal weight loss, is not necessarily beneficial and may have deleterious effects on offspring.

show abstract

Section: Discussionmentioning

confidence: 87%

A short-term transition from a high-fat diet to a normal-fat diet before pregnancy exacerbates female mouse offspring obesity

Olson

Rasmussen

et al. 2015

Int J Obes

View full text Add to dashboard Cite

show abstract

“…FAS activity was assessed in e-WAT since previous results have shown a downregulation of its activity in this specific fat pad in rats refed with SFA-MUFA diet (Marcelino et al, 2013). …”

Section: Methodsmentioning

confidence: 99%

Polyunsaturated Fatty Acids Stimulate De novo Lipogenesis and Improve Glucose Homeostasis during Refeeding with High Fat Diet

et al. 2017

Self Cite

View full text Add to dashboard Cite

Aims: The recovery of body weight after a period of caloric restriction is accompanied by an enhanced efficiency of fat deposition and hyperinsulinemia—which are exacerbated by isocaloric refeeding on a high fat diet rich in saturated and monounsaturated fatty acids (SFA-MUFA), and poor in polyunsaturated fatty acids (PUFA), and associated with a blunting of de novo lipogenesis in adipose tissue and liver. As high fat diets rich in PUFA have been shown to limit the excess fat deposition and improve glucose homeostasis, we investigated here the extent to which de novo lipogenesis in liver and adipose tissues (white and brown), as well as hepatic oxidative stress, are influenced by refeeding on diets rich in PUFA.Design: In rats calorically restricted for 14 days and refed for 14 days on isocaloric amounts of a high fat diet rich in lard (i.e., high SFA-MUFA) or in safflower and linseed oils (rich in PUFA), we investigated energy balance, body composition, glycemic profile, and the regulation of fatty acid synthase (rate-limiting enzyme of de novo lipogenesis) in liver, white and brown adipose tissue. We also evaluated oxidative stress in liver and skeletal muscle and markers of hepatic inflammation.Results: Rats refed the PUFA diet gained less lipids and more proteins compared to rats refed SFA-MUFA diet and showed lower amount of visceral and epididymal white adipose tissue, but increased depots of interscapular brown adipose tissue, with higher expression of the uncoupling protein 1. A significant increase in non-protein respiratory quotient and carbohydrate utilization was found in rats refed PUFA diet. Rats refed PUFA diet showed improved glucose homeostasis, as well as lower triglycerides and cholesterol levels. Fatty acid synthase activity was significantly higher in liver, white and brown adipose tissue, while lipid peroxidation and the degree of inflammation in the liver were significantly lower, in rats refed PUFA diet.Conclusions: When considering the composition of high fat diets for nutritional rehabilitation, the inclusion of PUFA could be useful for improving protein deposition and maintaining glucose homeostasis, while limiting lipid storage in adipose tissue and oxidative stress and inflammation in the liver.

show abstract

“…Recent work demonstrates that adipose tissue DNL is important in regulating glucose homeostasis ( 40 ). While glucose is thought to be the major precursor for DNL when mice are fed a diet high in carbohydrate, as much as one-third of TG/glycerol can be derived from nonglucose sources (i.e., glyceroneogenesis via PEPCK) ( 28 ).…”

Section: Discussionmentioning

confidence: 99%

Coupling of lipolysis and de novo lipogenesis in brown, beige, and white adipose tissues during chronic β3-adrenergic receptor activation

Mottillo

Balasubramanian

Lee

et al. 2014

Journal of Lipid Research

243

204

View full text Add to dashboard Cite

This article is available online at http://www.jlr.org Classic interscapular brown adipose tissue (BAT) is a thermogenic organ that has a high capacity for uncoupled oxidative metabolism ( 1 ). In contrast, white adipose tissue (WAT) has low oxidative capacity because its main function under normal conditions is to store excess energy as TGs. However, chronic stimulation by ␤ 3-adrenergic receptors ( ␤ 3-ARs) expands the oxidative capacity of WAT and converts it into a tissue resembling BAT. This phenomenon has been termed "browning" of white fat ( 2-4 ) and is marked by increased expression of oxidative genes, induction of uncoupling protein 1 (UCP1), and activation of oxidative metabolism ( 5 ). Importantly, lipolysis plays a central role in the catabolic activity of BAT and WAT. Acutely, mobilized FAs uncouple oxidative phosphorylation and provide fuel that supports both coupled and uncoupled respiration ( 6 ). Lipolysis also provides ligands for PPAR ␣ , which plays a central role in catabolic remodeling of WAT by upregulating oxidative metabolism and limiting FA-induced infl ammation ( 7,8 ). Indeed, several recent studies have demonstrated the importance of lipolysis in providing ligands for activation of PPAR target genes in BAT ( 9, 10 ), heart ( 11 ), liver ( 12, 13 ), and pancreatic ␤ cells ( 14 ).Abstract Chronic activation of ␤ 3-adrenergic receptors ( ␤ 3-ARs) expands the catabolic activity of both brown and white adipose tissue by engaging uncoupling protein 1 (UCP1)-dependent and UCP1-independent processes. The present work examined de novo lipogenesis (DNL) and TG/glycerol dynamics in classic brown, subcutaneous "beige," and classic white adipose tissues during sustained ␤ 3-AR activation by CL 316,243 (CL) and also addressed the contribution of TG hydrolysis to these dynamics. CL treatment for 7 days dramatically increased DNL and TG turnover similarly in all adipose depots, despite great differences in UCP1 abundance. Increased lipid turnover was accompanied by the simultaneous upregulation of genes involved in FAS, glycerol metabolism, and FA oxidation. Inducible, adipocyte-specifi c deletion of adipose TG lipase (ATGL), the rate-limiting enzyme for lipolysis, demonstrates that TG hydrolysis is required for CL-induced increases in DNL, TG turnover, and mitochondrial electron transport in all depots. Interestingly, the effect of ATGL deletion on induction of specifi c genes involved in FA oxidation and synthesis varied among fat depots. Overall, these studies indicate that FAS and FA oxidation are tightly coupled in adipose tissues during chronic adrenergic activation, and this effect critically depends on the activity of adipocyte ATGL. -

show abstract

A Role for Adipose Tissue De Novo Lipogenesis in Glucose Homeostasis During Catch-up Growth

Cited by 48 publications

References 38 publications

A short-term transition from a high-fat diet to a normal-fat diet before pregnancy exacerbates female mouse offspring obesity

A short-term transition from a high-fat diet to a normal-fat diet before pregnancy exacerbates female mouse offspring obesity

Polyunsaturated Fatty Acids Stimulate De novo Lipogenesis and Improve Glucose Homeostasis during Refeeding with High Fat Diet

Coupling of lipolysis and de novo lipogenesis in brown, beige, and white adipose tissues during chronic β3-adrenergic receptor activation

Contact Info

Product

Resources

About