Bifidobacterium animalis subsp. lactis BB-12 Has Effect Against Obesity by Regulating Gut Microbiota in Two Phases in Human Microbiota-Associated Rats

Bifidobacterium animalis subsp. lactis BB-12 (BB-12) is an extensively studied probiotics species, which has been reported to improve the human gut microbiota. This study aimed to confirm the effects of BB-12 on high-fat diet (HFD)-induced gut microbiota disorders. The probiotic BB-12 was consumed by human microbiota-associated rats and changes in gut microbiota were compared using next generation sequencing of the fecal samples collected from the normal chow group, the HFD group, and the BB-12-supplemented group. The enterotypes switched from Prevotella dominant to Akkermansia dominant as a result of switching diet from normal chow to HFD. BB-12 conferred protection on the gut microbiota composition of the rats by increasing the abundance of Prevotella and decreasing the abundance of Clostridium, Blautia, and Bacteroides in 0–3 weeks. In addition, Prevotella-dominant enterotype was maintained, which provides improve obesity effects. A decrease in body weight and the Firmicutes/Bacteroidetes ratio were also observed at week 3. While in 4–8 weeks, the enrichment of short-chain fatty acids-producing bacteria such as Eubacterium and Parabacteroides and probiotics such as Bifidobacterium was observed. The results revealed that BB-12 against obesity by regulating gut microbiota in two phases. After a short-term intervention, BB-12 supplementation suppressed the transition from the healthy to obesity state by protecting Prevotella-dominant enterotype, whereas after a long-term intervention, BB-12 ameliorates obesity by enriching beneficial bacteria in the gut.

Prelog Chow groups of self-products of degenerations of cubic threefolds

It is unknown whether smooth cubic threefolds have an (integral Chow-theoretic) decomposition of the diagonal, or whether they are stably rational or not in general. As a first step towards making progress on these questions, we compute the (saturated numerical) prelog Chow group of the self-product of a certain degeneration of cubic threefolds.

Algebraic cycles and Lehn–Lehn–Sorger–van Straten eightfolds

This article is about Lehn–Lehn–Sorger–van Straten eightfolds $Z$ and their anti-symplectic involution $\iota$ . When $Z$ is birational to the Hilbert scheme of points on a K3 surface, we give an explicit formula for the action of $\iota$ on the Chow group of $0$ -cycles of $Z$ . The formula is in agreement with the Bloch–Beilinson conjectures and has some non-trivial consequences for the Chow ring of the quotient.

Sprague Dawley Rats Gaining Weight on a High Energy Diet Exhibit Damage to Taste Tissue Even after Return to a Healthy Diet

Many reports detail taste dysfunction in humans and animals with obesity. For example, mice consuming an obesogenic diet for a short period have fewer taste buds than their lean littermates. Further, rats with diet-induced obesity (DIO) show blunted electrophysiological responses to taste in the brainstem. Here, we studied the effects of high energy diet (HED)-induced peripheral taste damage in rats, and whether this deficiency could be reversed by returning to a regular chow diet. Separate groups of rats consumed a standard chow diet (Chow), a HED for 10 weeks followed by a return to chow (HED/chow), or a HED for 10 weeks followed by a restricted HED that was isocaloric with consumption by the HED/chow group (HED/isocal). Fungiform taste papilla (FP) and circumvallate taste bud abundance were quantified several months after HED groups switched diets. Results showed that both HED/chow and HED/isocal rats had significantly fewer FP and lower CV taste bud abundance than control rats fed only chow. Neutrophil infiltration into taste tissues was also quantified, but did not vary with treatment on this timeline. Finally, the number of cells undergoing programmed cell death, measured with caspase-3 staining, inversely correlated with taste bud counts, suggesting taste buds may be lost to apoptosis as a potential mechanism for the taste dysfunction observed in obesity. Collectively, these data show that DIO has lasting deleterious effects on the peripheral taste system, despite a change from a HED to a healthy diet, underscoring the idea that obesity rather than diet predicts damage to the taste system.

Nonproper intersection products and generalized cycles

We develop intersection theory in terms of the $${{\mathscr {B}}}$$ B -group of a reduced analytic space. This group was introduced in a previous work as an analogue of the Chow group; it is generated by currents that are direct images of Chern forms and it contains all usual cycles. However, contrary to Chow classes, the $${{\mathscr {B}}}$$ B -classes have well-defined multiplicities at each point. We focus on a $${{\mathscr {B}}}$$ B -analogue of the intersection theory based on the Stückrad–Vogel procedure and the join construction in projective space. Our approach provides global $${{\mathscr {B}}}$$ B -classes which satisfy a Bézout theorem and have the expected local intersection numbers. We also introduce $${{\mathscr {B}}}$$ B -analogues of more classical constructions of intersections using the Gysin map of the diagonal. These constructions are connected via a $${{\mathscr {B}}}$$ B -variant of van Gastel’s formulas. Furthermore, we prove that our intersections coincide with the classical ones on cohomology level.

ON THE CHOW RING OF CERTAIN LEHN–LEHN–SORGER–VAN STRATEN EIGHTFOLDS

We consider a 10-dimensional family of Lehn–Lehn–Sorger–van Straten hyperkähler eightfolds, which have a non-symplectic automorphism of order 3. Using the theory of finite-dimensional motives, we show that the action of this automorphism on the Chow group of 0-cycles is as predicted by the Bloch–Beilinson conjectures. We prove a similar statement for the anti-symplectic involution on varieties in this family. This has interesting consequences for the intersection product of the Chow ring of these varieties.

Abnormal Glucose Metabolism in Male Mice Offspring Conceived by in vitro Fertilization and Frozen-Thawed Embryo Transfer

Frozen and thawed embryo transfer (FET) is currently widely applied in routine assisted reproductive technology (ART) procedure. It is of great necessity to assess the safety of FET and investigate the long-term effect including glucose metabolism on FET-conceived offspring. The mouse model is a highly efficient method to figure out the relationship between the process of FET and offspring health. In this study, we obtained mouse offspring of natural conception (NC), in vitro fertilization (IVF), and FET. Glucose and insulin tolerance test (GTT/ITT) were performed on both chow fed or high fat diet (HFD) fed offspring to examine the glucose metabolism status. We detected hepatic PI3K/AKT pathway by western blotting and transcriptome status by RNA-sequencing. Impaired glucose tolerance (IGT) and decreased insulin tolerance were occurred in FET conceived male offspring. After challenged with the HFD-fed, male offspring in FET group performed earlier and severer IGT than IVF group. Furthermore, higher HOMA-IR index and higher serum insulin level post glucose injected in FET-chow group suggested the insulin resistance status. The PI3K/AKT signaling pathway, the major pathway of insulin in the liver, were also disrupted in FET group. Transcriptomics of the liver reveals significantly downregulated in glucose metabolic process and insulin resistance in the FET-chow group. In our study, FET-conceived male mouse offspring presented glucose metabolism dysfunction mainly manifesting insulin resistance. The hepatic insulin signaling pathway were in concordance with reduced glycogen synthesis, increased glycolysis and enhanced gluconeogenesis status in FET-conceived male offspring.

On the dimension of voisin sets in the moduli space of abelian varieties

We study the subsets $$V_k(A)$$ V k ( A ) of a complex abelian variety A consisting in the collection of points $$x\in A$$ x ∈ A such that the zero-cycle $$\{x\}-\{0_A\}$$ { x } - { 0 A } is k-nilpotent with respect to the Pontryagin product in the Chow group. These sets were introduced recently by Voisin and she showed that $$\dim V_k(A) \le k-1$$ dim V k ( A ) ≤ k - 1 and $$\dim V_k(A)$$ dim V k ( A ) is countable for a very general abelian variety of dimension at least $$2k-1$$ 2 k - 1 . We study in particular the locus $${\mathcal {V}}_{g,2}$$ V g , 2 in the moduli space of abelian varieties of dimension g with a fixed polarization, where $$V_2(A)$$ V 2 ( A ) is positive dimensional. We prove that an irreducible subvariety $${\mathcal {Y}} \subset {\mathcal {V}}_{g,2}$$ Y ⊂ V g , 2 , $$g\ge 3$$ g ≥ 3 , such that for a very general $$y \in {\mathcal {Y}}$$ y ∈ Y there is a curve in $$V_2(A_y)$$ V 2 ( A y ) generating A satisfies $$\dim {\mathcal {Y}}\le 2g - 1.$$ dim Y ≤ 2 g - 1 . The hyperelliptic locus shows that this bound is sharp.

Hyperglycemia compromises the ischemia-provoked dedifferentiation of cerebral pericytes through p21–SOX2 signaling in high-fat diet-induced murine model

Aim: Diabetes-related cerebral small vessel disease (CSVD) causes neurological deficits. Patients with diabetes showed pericyte loss as a hallmark of retinopathy. Cerebral pericytes, which densely localize around brain capillaries, are quiescent stem cells regulating regeneration of brain and may have a role in CSVD development. This study investigated whether diabetes impairs ischemia-provoked dedifferentiation of pericytes. Methods: A murine high-fat diet (HFD)-induced diabetes model was used. After cerebral ischemia induction in the mice, pericytes were isolated and grown for a sphere formation assay. Results: The sphere counts from the HFD group were lower than those in the chow group. As the spheres formed, pericyte marker levels decreased and SOX2 levels increased gradually in the chow group, but not in the HFD group. Before sphere formation, pericytes from the HFD group showed high p21 levels. The use of a p21 inhibitor rescued the reduction of sphere counts in the HFD group. At cellular level, hyperglycemia-induced ROS increased the level of p21 in cerebral pericytes. The p21-SOX2 signaling was then activated after oxygen-glucose deprivation. Conclusion: HFD-induced diabetes compromises the stemness of cerebral pericytes by altering p21–SOX2 signaling. These results provide evidence supporting the role of pericytes in diabetes-related CSVD and subsequent cerebral dysfunction.