Adaptations to fasting in a terrestrial mustelid, the sable (Martes zibellina)

Mustonen, Anne‐Mari; Puukka, M.; Saarela, Seppo; Paakkonen, Tommi; Aho, Jari; Nieminen, Petteri

doi:10.1016/j.cbpa.2006.03.008

Cited by 26 publications

(33 citation statements)

References 34 publications

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“…Fasting declines in T 3 and T 4 have also been documented for king penguins during both the breeding and molting seasons (98,101). Hibernating black and brown bears as well as fasting canids (raccoon dog, grey wolf, and arctic fox) and mustelids (sable, badger, and mink) likewise experience significant decreases in T 3 and/or T 4 (23,136,193,250,267,391,393,474). In contrast to these examples of declines in thyroid hormone levels during fasting, in other species T 3 and/or T 4 are maintained, elevated, or fluctuate during the fasting phase, likely reflecting the complexity of thyroid hormone action on peripheral tissues.…”

Section: Thyroid Hormonesmentioning

confidence: 95%

“…5) (187,383,394,436). Within 48,48, and 96 h after the start of a fast, liver glycogen is depleted by 50%, 67%, and 70%, respectively, for the insectivorus bat Molossus molossus, the American marten Martes americana, and the sable Martes zibellina (186,393,408). For rodent hibernators, glycogen reserves decline during torpor bouts and are then replenished via gluconeogenesis during interbout arousals (198,199,505).…”

Section: Substrate Utilization During Fasting Glycogenmentioning

confidence: 97%

“…A 4-day fast increased plasma cortisol level by 160% for the sable (393). Upon entrance into Phase III, corticosterone levels in laboratory rats had risen by 19-fold (100).…”

Section: Glucocorticoidsmentioning

confidence: 97%

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Integrative Physiology of Fasting

Secor

Carey

2016

Comprehensive Physiology

138

144

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Extended bouts of fasting are ingrained in the ecology of many organisms, characterizing aspects of reproduction, development, hibernation, estivation, migration, and infrequent feeding habits. The challenge of long fasting episodes is the need to maintain physiological homeostasis while relying solely on endogenous resources. To meet that challenge, animals utilize an integrated repertoire of behavioral, physiological, and biochemical responses that reduce metabolic rates, maintain tissue structure and function, and thus enhance survival. We have synthesized in this review the integrative physiological, morphological, and biochemical responses, and their stages, that characterize natural fasting bouts. Underlying the capacity to survive extended fasts are behaviors and mechanisms that reduce metabolic expenditure and shift the dependency to lipid utilization. Hormonal regulation and immune capacity are altered by fasting; hormones that trigger digestion, elevate metabolism, and support immune performance become depressed, whereas hormones that enhance the utilization of endogenous substrates are elevated. The negative energy budget that accompanies fasting leads to the loss of body mass as fat stores are depleted and tissues undergo atrophy (i.e., loss of mass). Absolute rates of body mass loss scale allometrically among vertebrates. Tissues and organs vary in the degree of atrophy and downregulation of function, depending on the degree to which they are used during the fast. Fasting affects the population dynamics and activities of the gut microbiota, an interplay that impacts the host's fasting biology. Fasting-induced gene expression programs underlie the broad spectrum of integrated physiological mechanisms responsible for an animal's ability to survive long episodes of natural fasting.

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Section: Thyroid Hormonesmentioning

confidence: 95%

Section: Substrate Utilization During Fasting Glycogenmentioning

confidence: 97%

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Integrative Physiology of Fasting

Secor

Carey

2016

Comprehensive Physiology

138

144

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“…The depletion of n-3 PUFA has been proposed to favor FA and triacylglycerol (TAG) synthesis over hydrolysis and FA oxidation, and may impair lipid export from the liver by suppressing very-low-density lipoprotein (VLDL) secretion [9]. The most consistent endocrine responses associated with food deprivation in mustelids include decreased concentrations of plasma leptin, insulin and triiodothyronine (T 3 ) [12,16], while hematological changes suggesting immunosuppression have been reported [6,17]. The human NAFLD presents significant similarities in phenotype to the fasting-induced fatty liver in mustelids [15], despite the different principal correlates, i.e.…”

Section: Introductionmentioning

confidence: 97%

Rapid Development of Fasting‐Induced Hepatic Lipidosis in the American Mink (Neovison vison): Effects of Food Deprivation and Re‐Alimentation on Body Fat Depots, Tissue Fatty Acid Profiles, Hematology and Endocrinology

Rouvinen‐Watt

Mustonen

Conway

et al. 2009

Lipids

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Hepatic lipidosis is a common pathological finding in the American mink (Neovison vison) and can be caused by nutritional imbalance due to obesity or rapid body weight loss. The objectives of the present study were to investigate the timeline and characterize the development of hepatic lipidosis in mink in response to 0-7 days of food deprivation and liver recovery after 28 days of re-feeding. We report here the effects on hematological and endocrine variables, body fat mobilization, the development of hepatic lipidosis and the alterations in the liver lipid classes and tissue fatty acid (FA) sums. Food deprivation resulted in the rapid mobilization of body fat, most notably visceral, causing elevated hepatosomatic index and increased liver triacylglycerol content. The increased absolute amounts of liver total phospholipids and phosphatidylcholine suggested endoplasmic reticulum stress. The hepatic lipid infiltration and the altered liver lipid profiles were associated with a significantly reduced proportion of n-3 polyunsaturated FA (PUFA) in the livers and the decrease was more evident in the females. Likewise, re-feeding of the female mink resulted in a more pronounced recovery of the liver n-3 PUFA. The rapid decrease in the n-3/n-6 PUFA ratio in response to food deprivation could trigger an inflammatory response in the liver. This could be a key contributor to the pathophysiology of fatty liver disease in mink influencing disease progression.

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“…Food deprivation has been shown to induce simple steatosis in mink and other carnivores (Bjornvad et al 2004;Mustonen et al 2005Mustonen et al , 2006Armstrong and Blanchard 2009;Mustonen et al 2009;Nieminen et al 2009). In the mink of the current study, the reported liver lipid content for the 0-1 day fasted and re-fed groups was 5-6 %, while it increased to >13 % for the mink fasted for 3 days, and to 19-20 % in the 5-7 days fasted groups (Rouvinen-Watt et al 2010).…”

Section: Discussionmentioning

confidence: 94%

Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis

et al. 2014

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We investigated the presence of inflammatory signs in the progression of fatty liver disease induced by fasting. Sixty standard black American mink (Neovison vison) were fasted for 0, 1, 3, 5, or 7 days and one group for 7 days followed by re-feeding for 28 days. Liver sections were evaluated histologically and liver mRNA levels indicating endoplasmic reticulum (ER) stress, adipogenic transformation, and inflammation were assessed by quantitative real-time PCR. After 3 days of fasting, the mink had developed moderate liver steatosis. Increased hyaluronan reactivity in lymphocytic foci but no Mallory-Denk bodies were seen in livers of the mink fasted for 5-7 days. Up-regulation of glucose-regulated protein, 78 kDa was observed on day 7 indicating ER stress, especially in the females. Liver lipoprotein lipase and monocyte chemoattractant protein 1 mRNA levels increased in response to 5-7 days of food deprivation, while tumor necrosis factor α (TNF-α) was the highest in the mink fasted for 5 days. The expression of the genes of interest, except for TNF-α, correlated with each other and with the liver fat content. The mRNA levels were found to change more rapidly below n-3/n-6 polyunsaturated fatty acid ratio threshold of 0.15. Following re-feeding, hepatocyte morphology and mRNA abundance returned to pre-fasting levels. Within the studied timeframe, evidence for ER stress, adipogenic transformation, and liver inflammation suggested incipient transition from steatosis to steatohepatitis with potential for development of more severe liver disease. This may present a possibility to influence disease progression before histologically observable steatohepatitis.

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Adaptations to fasting in a terrestrial mustelid, the sable (Martes zibellina)

Cited by 26 publications

References 34 publications

Integrative Physiology of Fasting

Integrative Physiology of Fasting

Rapid Development of Fasting‐Induced Hepatic Lipidosis in the American Mink (Neovison vison): Effects of Food Deprivation and Re‐Alimentation on Body Fat Depots, Tissue Fatty Acid Profiles, Hematology and Endocrinology

Evidence of endoplasmic reticulum stress and liver inflammation in the American mink Neovison vison with benign hepatic steatosis

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