Adipose-Derived Factors During Nutritional Transitions

Abstract

It is now commonly accepted that white adipocytes actively secrete a wide range of bioactive molecules including leptin, adiponectin, resistin and many other signals. These adipose-derived factors are mainly influenced by nutritional transitions. This review addresses essentially the differential regulation and role of animal adipose-secreted products in regulating metabolic, endocrine and behavioral responses during prolonged fasting. When reaching a low adiposity threshold, animals enter late fasting characterized by elevated rates of protein degradation while lipid utilization decreases. Low NEFA levels in late fasting could affect PPAR activation and the management of body reserves, thus promoting food seeking behavior. Low leptin levels are also likely involved in the efficient mobilization of energy stores and in the induction of strong rises in hypothalamic orexigenic neuropeptides in late fasting. This effect is prevented by leptin perfusion. During fasting, adiponectin reduced levels could be related to its ability to signal nutritional and/or metabolic changes, to promote energy preservation or to prepare the body to efficiently restore body weight in case of refeeding while resistin low levels could constitute an adipose status sensor and/or improve glucose homeostasis. The fasting-induced changes of other signals during the fed/fasted/refed transitions are also briefly discussed.

Exacerbated oxidative stress in the fasting liver according to fuel partitioning

“…Peripheral metabolic sensing mechanisms are known to be conveyed to the central integrating centers via both humoral and neuronal routes . In previous studies, we hypothesized that the alarm signal , which induces feeding behavior in P3 of fasting, involves humoral signals related to metabolic changes, such as leptin and/or apolipoprotein A‐IV . In addition to these previous results, the current study suggests that liver impairments/dysfunctions during P3 could also trigger or be perceived as a signal, involving either circulating factors that could be complementary to those previously reported , or another (e.g., neural) signaling route (Fig.…”

“…Capabilities for responding/resisting to food deprivation largely differ not only between species, but also between individuals of the same species, independently of the obvious influence of fasting duration. Great similarities nevertheless exist between the metabolic expression of starvation in extremely malnourished dying patients and long‐term fasted healthy persons , and wild and laboratory animals. In particular, body proteins are spared while carbohydrate and lipid reserves are successively utilized during the so‐called phase 1 and phase 2 of fasting (P1 and P2).…”

Protracted Impairment of Maternal Metabolic Health in Mouse Dams Following Pregnancy Exposure to a Mixture of Low Dose Endocrine-Disrupting Chemicals, a Pilot Study

“…MIX dams did not show altered serum adipokines: adiponectin [104], insulin [90], monocyte chemoattractant protein-1 (MCP-1) [105], plasminogen activator inhibitor-1 total (PAI-1 Total) [106], or resistin [107], in response to exposures. Fasting and glucose tolerance tests have been shown to alter adipokine levels, which might have led to the lack of adipokine effects seen post-glucose-tolerance test in MIX dams [108,109]. Consequently, future studies are needed to assess adipokine levels at baseline, not after fasting and subsequent glucose-tolerance testing.…”

Physiological response to extreme fasting in subantarctic fur seal (Arctocephalus tropicalis) pups: metabolic rates, energy reserve utilization, and water fluxes

“…Furthermore, protein conservation has been shown to depend upon the level of fatty acid oxidation (13), a metabolic pathway that remains predominant regardless of nutritional transitions in subantarctic fur seal pups. In addition, NEFAs and their metabolites constitute endogenous ligands for peroxysome proliferators-activated receptors (14). In particular, NEFA-activated peroxysome proliferators-activated receptor-␣ increase fatty acid oxidation and ketone body production, and thus represent a "fasting-lipidoxidation-glucose-sparing" regulator at the expense of muscle protein catabolism (37).…”