Academic interests
Higher education and employment history
- PhD, University of Oslo, Norway
- MSc Molecular Nutrition and Toxicology, Wageningen University and Research Center, the Netherlands
- MSc Pharmacy, Medical University Plovdiv, Bulgaria
Publications
-
-
Pandey, Deepak; Doncheva, Atanaska Ivanova; Sapkota, Rumakanta; Jüterbock, Alexander Oliver; Viswanath, Kiron & Dalen, Knut Tomas
[Show all 7 contributors for this article]
(2025).
Dietary inclusions of the brown macroalgae, Ascophyllum nodosum and Fucus vesiculosus, favourably modulate fat deposition and the caecal microbiome of obese mice.
Food Bioscience.
ISSN 2212-4292.
68.
doi:
10.1016/j.fbio.2025.106590.
Full text in Research Archive
Show summary
Effective preventive measures are needed to lower the global incidence of obesity in humans. We investigated whether the dietary inclusions of brown macroalgae Ascophyllum nodosum (AN) or Fucus vesiculosus (FV) prevent diet-associated obesity development in mice by modulating the gut microbiome and body composition. Female C57BL/6J mice were fed a low-fat control, high-fat (HF), or HF diet with 5 % inclusion of whole AN or FV biomass for 12 weeks. Body composition, whole-body energy metabolism, caecal microbiome, and liver transcriptomics were evaluated. Mice fed AN and FV-added HF diets had lower gonadal (∼30 %), subcutaneous (∼25 %), and total (∼40 %) fat mass compared to the mice fed the HF diet, although the differences were statistically non-significant. Macroalgae-supplemented diet groups had reduced Firmicutes: Bacteroidota ratios and lower abundances of obesity-associated bacterial genera, including Lachnoclostridium, Lachnospiraceae, Lactococcus, Romboutsia, and Tuzzerella in the caecal contents, compared to the HF diet group (more prominently with FV-supplementation). These bacteria were found to be positively associated with fat mass gain. On the other hand, macroalgal addition promoted certain leanness-associated and short-chain fatty acids-producing bacteria, where FV-addition most prominently enriched Alistipes, Akkermansia, Muribaculum, and Oscillospiraceae NK4A214 group, while AN-addition highly promoted the Bacteroides. This study shows that dietary inclusion of AN or FV in the HF diet promotes a unique and healthier gut microbiota and lowers the HF diet-associated fat mass gain in mice.
-
Meen, Astri Jeanette; Doncheva, Atanaska Ivanova; Böttcher, Yvonne; Dankel, Simon N; Hoffmann, Anne & Blüher, Matthias
[Show all 16 contributors for this article]
(2023).
Obesity Is Associated with Distorted Proteoglycan Expression in Adipose Tissue.
International Journal of Molecular Sciences.
ISSN 1661-6596.
24(8).
doi:
10.3390/ijms24086884.
Full text in Research Archive
Show summary
Proteoglycans are central components of the extracellular matrix (ECM) and binding partners for inflammatory chemokines. Morphological differences in the ECM and increased inflammation are prominent features of the white adipose tissues in patients with obesity. The impact of obesity and weight loss on the expression of specific proteoglycans in adipose tissue is not well known. This study aimed to investigate the relationship between adiposity and proteoglycan expression. We analyzed transcriptomic data from two human bariatric surgery cohorts. In addition, RT-qPCR was performed on adipose tissues from female and male mice fed a high-fat diet. Both visceral and subcutaneous adipose tissue depots were analyzed. Adipose mRNA expression of specific proteoglycans, proteoglycan biosynthetic enzymes, proteoglycan partner molecules, and other ECM-related proteins were altered in both human cohorts. We consistently observed more profound alterations in gene expression of ECM targets in the visceral adipose tissues after surgery (among others VCAN (p = 0.000309), OGN (p = 0.000976), GPC4 (p = 0.00525), COL1A1 (p = 0.00221)). Further, gene analyses in mice revealed sex differences in these two tissue compartments in obese mice. We suggest that adipose tissue repair is still in progress long after surgery, which may reflect challenges in remodeling increased adipose tissues. This study can provide the basis for more mechanistic studies on the role of proteoglycans in adipose tissues in obesity.
-
Doncheva, Atanaska Ivanova; Li, Yuchuan; Khanal, Prabhat; Hjorth, Marit; Kolset, Svein Olav & Norheim, Frode Amador
[Show all 8 contributors for this article]
(2023).
Altered hepatic lipid droplet morphology and lipid metabolism in fasted Plin2-null mice.
Journal of Lipid Research.
ISSN 0022-2275.
64(12).
doi:
10.1016/j.jlr.2023.100461.
Full text in Research Archive
Show summary
Perilipin 2 (Plin2) binds to the surface of hepatic lipid droplets (LDs) with expression levels that correlate with triacylglyceride (TAG) content. We investigated if Plin2 is important for hepatic LD storage in fasted or high-fat diet-induced obese Plin2+/+ and Plin2−/− mice. Plin2−/− mice had comparable body weights, metabolic phenotype, glucose tolerance, and circulating TAG and total cholesterol levels compared with Plin2+/+ mice, regardless of the dietary regime. Both fasted and high-fat fed Plin2−/− mice stored reduced levels of hepatic TAG compared with Plin2+/+ mice. Fasted Plin2−/− mice stored fewer but larger hepatic LDs compared with Plin2+/+ mice. Detailed hepatic lipid analysis showed substantial reductions in accumulated TAG species in fasted Plin2−/− mice compared with Plin2+/+ mice, whereas cholesteryl esters and phosphatidylcholines were increased. RNA-Seq revealed minor differences in hepatic gene expression between fed Plin2+/+ and Plin2−/− mice, in contrast to marked differences in gene expression between fasted Plin2+/+ and Plin2−/− mice. Our findings demonstrate that Plin2 is required to regulate hepatic LD size and storage of neutral lipid species in the fasted state, while its role in obesity-induced steatosis is less clear.
-
Doncheva, Atanaska Ivanova; Romero, Silvana Angelica Troncoso; Ramirez-Garrastacho, Manuel; Lee-Ødegård, Sindre; Kolnes, Kristoffer Jensen & Tangen, Daniel S.
[Show all 11 contributors for this article]
(2022).
Extracellular vesicles and microRNAs are altered in response to exercise, insulin sensitivity and overweight.
Acta Physiologica.
ISSN 1748-1708.
236(4).
doi:
10.1111/apha.13862.
Full text in Research Archive
Show summary
Abstract: Extracellular vesicles induced by exercise have emerged as potential mediators of tissue crosstalk. Extracellular vesicles and their cargo miRNAs have been linked to dysglycemia and obesity in animal models, but their role in humans is unclear. Aim: The aim of the study was to characterize the miRNA content in plasma extracellular vesicle isolates after acute and long-term exercise and to study associations between extracellular vesicle miRNAs, mRNA expression in skeletal muscle and adipose tissue, and cardiometabolic risk factors. Methods: Sedentary men with or without dysglycemia and overweight underwent an acute bicycle test and a 12-week exercise intervention with extensive metabolic phenotyping. Gene expression in m. vastus lateralis and subcutaneous adipose tissue was measured with RNA sequencing. Extracellular vesicles were purified from plasma with membrane affinity columns or size exclusion chromatography. Results: Extracellular vesicle miRNA profiling revealed a transient increase in the number of miRNAs after acute exercise. We identified miRNAs, such as miR-652-3p, that were associated to insulin sensitivity and adiposity. By performing explorative association analyses, we identified two miRNAs, miR-32-5p and miR-339-3p, that were strongly correlated to an adipose tissue macrophage signature. Conclusion: Numerous miRNAs in plasma extracellular vesicle isolates were increased by exercise, and several miRNAs correlated to insulin sensitivity and adiposity. Our findings warrant future studies to characterize exercise-induced extracellular vesicles and cargo miRNA to clarify where exercise-induced extracellular vesicles originate from, and to determine whether they influence metabolic health or exercise adaptation.
-
Hjorth, Marit; Doncheva, Atanaska Ivanova; Norheim, Frode Amador; Ulven, Stine Marie; Holven, Kirsten Bjørklund & Sæther, Thomas
[Show all 7 contributors for this article]
(2022).
Consumption of salmon fishmeal increases hepatic cholesterol content in obese C57BL/6 J mice.
European Journal of Nutrition.
ISSN 1436-6207.
61,
p. 4027–4043.
doi:
10.1007/s00394-022-02930-y.
Full text in Research Archive
Show summary
Abstract
Purpose
By-products from farmed fish contain large amounts of proteins and may be used for human consumption. The purpose of this study was to investigate cardiometabolic effects and metabolic tolerance in mice consuming fishmeal from salmon by-products, salmon filet or beef.
Methods
Female C57BL/6J mice were fed chow, as a healthy reference group, or a high-fat diet for 10 weeks to induce obesity and glucose intolerance. Obese mice were subsequently given isocaloric diets containing 50% of the dietary protein from salmon fishmeal, salmon filet or beef for 10 weeks. Mice were subjected to metabolic phenotyping, which included measurements of body composition, energy metabolism in metabolic cages and glucose tolerance. Lipid content and markers of hepatic toxicity were determined in plasma and liver. Hepatic gene and protein expression was determined with RNA sequencing and immunoblotting.
Results
Mice fed fishmeal, salmon filet or beef had similar food intake, energy consumption, body weight gain, adiposity, glucose tolerance and circulating levels of lipids and hepatic toxicity markers, such as p-ALT and p-AST. Fishmeal increased hepatic cholesterol levels by 35–36% as compared to salmon filet (p = 0.0001) and beef (p = 0.005). This was accompanied by repressed expression of genes involved in steroid and cholesterol metabolism and reduced levels of circulating Pcsk9.
Conclusion
Salmon fishmeal was well tolerated, but increased hepatic cholesterol content. The high cholesterol content in fishmeal may be responsible for the effects on hepatic cholesterol metabolism. Before introducing fishmeal from salmon by-products as a dietary component, it may be advantageous to reduce the cholesterol content in fishmeal.
Introduction
-
Doncheva, Atanaska Ivanova; Norheim, Frode Amador; Hjorth, Marit; Grujic, Mirjana; Paivandy, Aida & Dankel, Simon N
[Show all 14 contributors for this article]
(2021).
Serglycin Is Involved in Adipose Tissue Inflammation in Obesity.
Journal of Immunology.
ISSN 0022-1767.
208(1),
p. 121–132.
doi:
10.4049/jimmunol.2100231.
Full text in Research Archive
Show summary
Chronic local inflammation of adipose tissue is an important feature of obesity. Serglycin is a proteoglycan highly expressed by various immune cell types known to infiltrate adipose tissue under obese conditions. To investigate if serglycin expression has an impact on diet-induced adipose tissue inflammation, we subjected Srgn+/+ and Srgn−/− mice (C57BL/6J genetic background) to an 8-wk high-fat and high-sucrose diet. The total body weight was the same in Srgn+/+ and Srgn−/− mice after diet treatment. Expression of white adipose tissue genes linked to inflammatory pathways were lower in Srgn−/− mice. We also noted reduced total macrophage abundance, a reduced proportion of proinflammatory M1 macrophages, and reduced formation of crown-like structures in adipose tissue of Srgn−/− compared with Srgn+/+ mice. Further, Srgn−/− mice had more medium-sized adipocytes and fewer large adipocytes. Differentiation of preadipocytes into adipocytes (3T3-L1) was accompanied by reduced Srgn mRNA expression. In line with this, analysis of single-cell RNA sequencing data from mouse and human adipose tissue supports that Srgn mRNA is predominantly expressed by various immune cells, with low expression in adipocytes. Srgn mRNA expression was higher in obese compared with lean humans and mice, accompanied by an increased expression of immune cell gene markers. SRGN and inflammatory marker mRNA expression was reduced upon substantial weight loss in patients after bariatric surgery. Taken together, this study introduces a role for serglycin in the regulation of obesity-induced adipose inflammation.
-
Doncheva, Atanaska Ivanova
(2019).
Transcriptional Response of White Adipose Tissueto Withdrawal of Vitamin B3.
Molecular Nutrition & Food Research.
ISSN 1613-4125.
63.
doi:
10.1002/mnfr.201801100.
Full text in Research Archive
Show summary
Scope Distinct markers for mild vitamin B3 deficiency are lacking. To identify these, the molecular responses of white adipose tissue (WAT) to vitamin B3 withdrawal are examined. Methods and results A dietary intervention is performed in male C57BL/6JRccHsd mice, in which a diet without nicotinamide riboside (NR) is compared to a diet with NR at the recommended vitamin B3 level. Both diets contain low but adequate level of tryptophan. Metabolic flexibility and systemic glucose tolerance are analyzed and global transcriptomics, qRT-PCR, and histology of epididymal WAT (eWAT) are performed. A decreased insulin sensitivity and a shift from carbohydrate to fatty acid oxidation in response to vitamin B3 withdrawal are observed. This is consistent with molecular changes in eWAT, including an activated MEK/ERK signaling, a lowering of glucose utilization markers, and an increase in makers of fatty acid catabolism, possibly related to the consistent lower expression of mitochondrial electron transport complexes. The synthesis pathway of tetrahydropteridine (BH4), an essential cofactor for neurotransmitter synthesis, is transcriptionally activated. Genes marking these processes are technically validated. Conclusion The downregulation of Anp32a, Tnk2 and the upregulation of Mapk1, Map2k1, Qdpr, Mthfs, and Mthfsl are proposed as a WAT transcriptional signature marker for mild vitamin B3 deficiency.
-
Doncheva, Atanaska Ivanova
(2019).
High Dose of Dietary Nicotinamide Riboside Induces Glucose Intolerance and White Adipose Tissue Dysfunction in Mice Fed a Mildly Obesogenic Diet.
Nutrients.
doi:
10.3390/nu11102439.
Full text in Research Archive
Show summary
Nicotinamide riboside (NR) is a nicotinamide adenine dinucleotide (NAD+) precursor vitamin. The scarce reports on the adverse effects on metabolic health of supplementation with high-dose NR warrant substantiation. Here, we aimed to examine the physiological responses to high-dose NR supplementation in the context of a mildly obesogenic diet and to substantiate this with molecular data. An 18-week dietary intervention was conducted in male C57BL/6JRccHsd mice, in which a diet with 9000 mg NR per kg diet (high NR) was compared to a diet with NR at the recommended vitamin B3 level (control NR). Both diets were mildly obesogenic (40 en% fat). Metabolic flexibility and glucose tolerance were analyzed and immunoblotting, qRT-PCR and histology of epididymal white adipose tissue (eWAT) were performed. Mice fed with high NR showed a reduced metabolic flexibility, a lower glucose clearance rate and aggravated systemic insulin resistance. This was consistent with molecular and morphological changes in eWAT, including sirtuin 1 (SIRT1)-mediated PPARγ (proliferator-activated receptor γ) repression, downregulated AKT/glucose transporter type 4 (GLUT4) signaling, an increased number of crown-like structures and macrophages, and an upregulation of pro-inflammatory gene markers. In conclusion, high-dose NR induces the onset of WAT dysfunction, which may in part explain the deterioration of metabolic health.
View all works in NVA
Published
Oct. 18, 2019 12:53 PM
- Last modified
Feb. 26, 2026 10:42 AM
.jpg)