The effect of biological age on the metabolic responsiveness of mice fed a high-fat diet

Korou, Laskarina Maria; Doulamis, Ilias P.; Tzanetakou, Irene P.; Mikhailidis, Dimitri P.; Perrea, Despina

doi:10.1177/0023677213480768

Cited by 14 publications

(10 citation statements)

References 20 publications

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“…In animals, an HFD differentially influences body metabolism and metabolic disease with age. HFD feeding resulted in greater increases in body weight and serum total cholesterol and glucose levels in older mice compared with younger mice [ 30 ]. Our study suggests that consumption of an HFD by elderly men, who generally have low testosterone levels, may promote the development of metabolic syndrome.…”

Section: Discussionmentioning

confidence: 99%

Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

et al. 2020

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Background Testosterone deficiency in men is clinically associated with the development of metabolic syndrome, which manifests as obesity, hepatic steatosis, and type-2 diabetes. We investigated the effects of castration-induced testosterone deficiency on body adiposity and the expression of genes related to lipid metabolism and glucose uptake and androgen signaling in male rats fed a normal diet (ND) or a high-fat diet (HFD). Methods Changes in lipid and glucose metabolism and androgen signaling were investigated at physiological and molecular levels in the muscle, liver, and adipose tissues of non-castrated and castrated rats under ND or HFD feeding. Results Castration-induced testosterone deficiency predisposed animals on ND to early development of fatty liver by activating fatty acid (FA) synthesis, whereas HFD activated hepatic FA uptake CD36 expression, leading to the development of hepatic steatosis. In rats fed ND, castration induced muscle fat accumulation by activating CD36 expression. In the subcutaneous fat of ND-fed rats, castration increased adiposity and the expression of FA synthesis-related genes, but it decreased glucose transporter gene expression. In the abdominal fat of rats fed ND, castration increased adiposity by upregulating FA synthesis-related genes, and HFD promoted adiposity by inducing FA uptake, glucose transporter, and FA synthesis-related gene expression. In rats fed ND, castration decreased body growth and muscle weight and downregulated the expression of genes androgen signaling in the longissimus dorsi muscle. Conclusions Testosterone deficiency increases adiposity in a tissue-specific and diet-dependent manner. Testosterone deficiency decreases body and muscle weights and downregulates androgen signaling.

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Section: Discussionmentioning

confidence: 99%

Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

et al. 2020

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“…It is important to remember that obesity is a complex and multifactorial disease, and there are several factors that appear to influence its biomarkers such as gender [43], age [44], type of fatty acid offered [45], and duration of therapy [46]. Interestingly, our data showed that high-fat feeding during the 16 week period did not alter the content of pro-or antiinflammatory cytokines IL-10, IL-6, or TNF-α and respective receptors, nor did it alter the TLR4 protein expression levels in the liver (Table 4 and Figure 3).…”

Section: Discussionmentioning

confidence: 99%

Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice

Santamarina

Carvalho-Silva

Gomes

et al. 2015

The Journal of Nutritional Biochemistry

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Nonalcoholic fatty liver disease has been considered the hepatic manifestation of obesity. It is unclear whether supplementation with green tea extract rich in epigallocatechin-3-gallate (EGCG) influences the activity of mitochondrial respiratory chain complexes and insulin resistance in the liver. EGCG regulated hepatic mitochondrial respiratory chain complexes and was capable of improving lipid metabolism, attenuating insulin resistance in obese mice. Mice were divided into four groups: control diet+water (CW) or EGCG (CE) and hyperlipidic diet+water (HFW) or EGCG (HFE). All animals received water and diets ad libitum for 16 weeks. Placebo groups received water (0.1 ml/day) and EGCG groups (0.1 ml EGCG and 50 mg/kg/day) by gavage. Cytokines concentrations were obtained by ELISA, protein expression through Western blotting and mitochondrial complex enzymatic activity by colorimetric assay of substrate degradation. HFW increased body weight gain, adiposity index, retroperitoneal and mesenteric adipose tissue relative weight, serum glucose, insulin and Homeostasis Model Assessment of Basal Insulin Resistance (HOMA-IR); glucose intolerance was observed in oral glucose tolerance test (OGTT) as well as ectopic fat liver deposition. HFE group decreased body weight gain, retroperitoneal and mesenteric adipose tissue relative weight, HOMA-IR, insulin levels and liver fat accumulation; increased complexes II-III and IV and malate dehydrogenase activities and improvement in glucose uptake in OGTT and insulin sensitivity by increased protein expression of total AKT, IRα and IRS1. We did not find alterations in inflammatory parameters analyzed. EGCG was able to prevent obesity stimulating the mitochondrial complex chain, increasing energy expenditure, particularly from the oxidation of lipid substrates, thereby contributing to the prevention of hepatic steatosis and improved insulin sensitivity.

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“…There is also variability in change in total adipose tissue mass among different depots and mouse strains in response to HFD (371, 509). The age of animals at the onset of HFD feeding is yet another factor that can influence weight gain (51, 246, 517). HFD feeding is commonly associated with the development of insulin resistance and impaired glucose homeostasis in many models; however, the duration of HFD feeding and diet composition, including dietary fat source, influence not only body weight but also the timing of onset and severity of disturbed glucose regulation (54).…”

Section: Adiposity and Insulin Resistancementioning

confidence: 99%

Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

Burhans

Hagman

Kuzma

et al. 2018

Comprehensive Physiology

263

241

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The objective of this comprehensive review is to summarize and discuss the available evidence of how adipose tissue inflammation affects insulin sensitivity and glucose tolerance. Low-grade, chronic adipose tissue inflammation is characterized by infiltration of macrophages and other immune cell populations into adipose tissue, and a shift towards more pro-inflammatory subtypes of leukocytes. The infiltration of pro-inflammatory cells in adipose tissue is associated with an increased production of key chemokines such as C-C motif chemokine ligand 2, pro-inflammatory cytokines including tumor necrosis factor α and interleukins 1β and 6, as well as reduced expression of the key insulin sensitizing adipokine, adiponectin. In both rodent models and humans, adipose tissue inflammation is consistently associated with excess fat mass and insulin resistance. In humans, associations with insulin resistance are stronger and more consistent for inflammation in visceral as opposed to subcutaneous fat. Further, genetic alterations in mouse models of obesity that reduce adipose tissue inflammation are – almost without exception - associated with improved insulin sensitivity. However, a dissociation between adipose tissue inflammation and insulin resistance can be observed in very few rodent models of obesity as well as in humans following bariatric surgery- or low-calorie diet-induced weight loss, illustrating that the etiology of insulin resistance is multifactorial. Taken together, adipose tissue inflammation is a key factor in the development of insulin resistance and type 2 diabetes in obesity, along with other factors that likely include inflammation and fat accumulation in other metabolically active tissues.

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The effect of biological age on the metabolic responsiveness of mice fed a high-fat diet

Cited by 14 publications

References 20 publications

Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

Testosterone deficiency caused by castration increases adiposity in male rats in a tissue-specific and diet-dependent manner

Decaffeinated green tea extract rich in epigallocatechin-3-gallate prevents fatty liver disease by increased activities of mitochondrial respiratory chain complexes in diet-induced obesity mice

Contribution of Adipose Tissue Inflammation to the Development of Type 2 Diabetes Mellitus

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