In vivo imaging of lipid storage and regression in diet-induced obesity during nutrition manipulation

Bidar, Abdel Wahad; Ploj, Karolina; Lelliott, Christopher J.; Nelander, Karin; Winzell, Maria Sörhede; Böttcher, Gerhard; Oscarsson, Jan; Storlien, Leonard H; Hockings, Paul D.

doi:10.1152/ajpendo.00274.2012

Cited by 6 publications

(6 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to the lack of short-term changes in HLC on exposure to HFD formulas, a few weeks of dietary reversal from HFD60 to CD was sufficient to induce an effective decrease of HLC. This rapid response was also observed in another study that performed a dietary switch from an obesogenic to a control diet [48].…”

Section: Discussionsupporting

confidence: 66%

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

Soares

Duarte

Gruetter

2017

Magn Reson Mater Phy

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 66%

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

Soares

Duarte

Gruetter

2017

Magn Reson Mater Phy

View full text Add to dashboard Cite

show abstract

“…A comparison was then made with publications on B6N and B6J mice exposed to high fat diet (varying compositions) for a broadly similar time period (up to 6 months duration). The criteria used to identify relevant publications on Pubmed were the strain name (searching for C57BL/6N along returned 827 references; searching for C57BL/6J alone returned 11,819 references, March 2013) combined with key search terms such as glucose, body weight or steatosis a Males and females fed HFD (42 % kcal from fat) from 4 weeks of age for up to 12 weeks (current study) b Males and females fed HFD (35 % w/w as lipids) from 4 weeks of age for 15 and 35 weeks (Medrikova et al 2012) c Females fed HFD (45 % kcal from fat) from 10 weeks of age for 10 weeks (Brown et al 2012) d Females fed HFD (35 % w/w as fat) from 6 weeks of age for 10 weeks (Fenton et al 2009) e Males fed HFD (58 % kcal from fat) from 4 weeks of age for 11 weeks (Petro et al 2004) f Males fed HFD (33 % kcal from fat) from 5 weeks of age for 7 weeks (West et al 1992) g Males fed HFD (45 % kcal from fat) from 12 weeks of age for 8 weeks (de Wilde et al 2009) h Females fed HFD (cafeteria) from 8 weeks of age for 16 weeks (Bidar et al 2012) i Males fed HFD (60 % lipids) from 7 weeks of age for 24 weeks (Ma et al 2010) j Males fed HFD (35 % w/w as lipids) from 3 months of age for 8 weeks (Horakova et al 2012) k Males fed HFD (60 % kcal from fat) from 6 months of age for 10 weeks (Gilbert et al 2011) l Females fed HFD (15 % w/w from fat) from 7 weeks of age for 6 months (Murakami et al 1998) m Males fed HFD (59 % kcal from fat) from 3 months of age for 7 weeks (Guo et al 2009) n Males fed HFD (28 % w/w from fat) from 5 weeks of age for 8 weeks (Fukushima et al 2009) o Males fed HFD (15 % w/w as fat) for 30 weeks (Savard et al 2013) p Males fed HFD (58 % kcal from fat) from 2 months of age for 8 weeks (Rossmeisl et al 2003) q Males fed HFD (19 % w/w from fat) from 10 weeks of age for 18 weeks (Desmarchelier et al 2013) r Males fed HFD (42 % kcal from fat) from 4 weeks of age for 10 weeks (Tan et al 2011) s Males fed HFD (60 % kcal from fat) from 4 weeks of age for 13 weeks (Pini et al 2011) t Males fed HFD (45 % kcal from fat) from 6 weeks of age for 24 weeks (Trottier et al 2012) u Males fed HFD (21 % w/w from milk fat with increased sucrose) from 6 weeks of age for 20 weeks (Sundaresan et al 2011)…”

Section: Resultsmentioning

confidence: 99%

High-fat feeding rapidly induces obesity and lipid derangements in C57BL/6N mice

Podrini

Cambridge²,

Lelliott

et al. 2013

Mamm Genome

View full text Add to dashboard Cite

C57BL/6N (B6N) is becoming the standard background for genetic manipulation of the mouse genome. The B6N, whose genome is very closely related to the reference C57BL/6J genome, is versatile in a wide range of phenotyping and experimental settings and large repositories of B6N ES cells have been developed. Here, we present a series of studies showing the baseline characteristics of B6N fed a high-fat diet (HFD) for up to 12 weeks. We show that HFD-fed B6N mice show increased weight gain, fat mass, and hypercholesterolemia compared to control diet-fed mice. In addition, HFD-fed B6N mice display a rapid onset of lipid accumulation in the liver with both macro- and microvacuolation, which became more severe with increasing duration of HFD. Our results suggest that the B6N mouse strain is a versatile background for studying diet-induced metabolic syndrome and may also represent a model for early nonalcoholic fatty liver disease.Electronic supplementary materialThe online version of this article (doi:10.1007/s00335-013-9456-0) contains supplementary material, which is available to authorized users.

show abstract

“…Accumulation of visceral adipose tissue has previously been identified as a major driver of metabolic disease processes including insulin resistance and chronic inflammation [ 10 , 14 , 15 ]. The retroperitoneal adipose tissue (RpAT) examined in the present study belongs to the intra-abdominal, visceral fat depots, which are known to be enlarged by both diet- and prenatally-induced obesity [ 6 , 20 ]. In contrast, subcutaneous adipose tissue represents fat stored directly under the skin.…”

Section: Discussionmentioning

confidence: 99%

Metabolic programming of adipose tissue structure and function in male rat offspring by prenatal undernutrition

Thompson

Huber²,

Bedürftig³

et al. 2014

Nutr Metab (Lond)

View full text Add to dashboard Cite

BackgroundA number of different pathways to obesity with different metabolic outcomes are recognised. Prenatal undernutrition in rats leads to increased fat deposition in adulthood. However, the form of obesity is metabolically distinct from obesity induced through other pathways (e.g. diet-induced obesity). Previous rat studies have shown that maternal undernutrition during pregnancy led to insulin hyper-secretion and obesity in offspring, but not to systemic insulin resistance. Increased muscle and liver glycogen stores indicated that glucose is taken up efficiently, reflecting an active physiological function of these energy storage tissues. It is increasingly recognised that adipose tissue plays a central role in the regulation of metabolism and pathophysiology of obesity development. The present study investigated the cell size and endocrine responsiveness of subcutaneous and visceral adipose tissue from prenatally undernourished rats. We aimed to identify whether these adipose tissue depots contribute to the altered energy metabolism observed in these offspring.MethodsAdipocyte size was measured in both subcutaneous (ScAT) and retroperitoneal adipose tissue (RpAT) in male prenatally ad libitum fed (AD) or prenatally undernourished (UN) rat offspring. Metabolic responses were investigated in adipose tissue explants stimulated by insulin and beta3 receptor agonists ex vivo. Expression of markers of insulin signalling was determined by Western blot analyses. Data were analysed by unpaired t-test or Two Way ANOVA followed by Fisher’s PLSD post-hoc test, where appropriate.ResultsAdipocytes in offspring of undernourished mothers were larger, even at a lower body weight, in both RpAT and ScAT. The insulin response of adipose tissue was reduced in ScAT, and statistically absent in RpAT of UN rats compared with control. This lack of RpAT insulin response was associated with reduced expression of insulin signalling pathway proteins. Adrenergic receptor-driven lipolysis was observed in both adipose depots; however insulin failed to express its anti-lipolytic effect in RpAT in both, AD and UN offspring.ConclusionsMetabolic dysregulation in offspring of undernourished mothers is mediated by increased adipocyte size and reduced insulin responsiveness in both ScAT and especially in RpAT. These functional and morphological changes in adipocytes were accompanied by impaired activity of the insulin signalling cascade highlighting the important role of different adipose tissue depots in the pathogenesis of metabolic disorders.

show abstract

In vivo imaging of lipid storage and regression in diet-induced obesity during nutrition manipulation

Abstract: Bidar AW, Ploj K, Lelliott C, Nelander K, Winzell MS, Böttcher G, Oscarsson J, Storlien L, Hockings PD. In vivo imaging of lipid storage and regression in diet-induced obesity during nutrition manipulation.

Cited by 6 publications

References 53 publications

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

High-fat feeding rapidly induces obesity and lipid derangements in C57BL/6N mice

Metabolic programming of adipose tissue structure and function in male rat offspring by prenatal undernutrition

Contact Info

Product

Resources

About