KU4 inhibits adipocyte senescence in aged mice through necdin regulation of p53 activity.

Previously, we reported that KU4 (LKU4) ameliorates diet-induced metabolic disorders by regulating adipose tissue (AT) physiology. Since metabolic disorders and age-related pathological conditions mutually exacerbate each other, this study hypothesizes that LKU4 may protect against adipose senescence during aging. Thus, this study demonstrates that LKU4 administration suppresses age-related metabolic dysfunction and aging phenotypes in AT of 24-month-old mice.

Lactobacillus amylovorus KU4 induces adipose browning in obese mice by regulating PP4C.

We previously reported that Lactobacillus amylovorus KU4 (LKU4) promotes adipocyte browning in mice fed a high-fat diet (HFD mice) in part by remodeling the PPARγ transcription complex. However, the mechanism through which LKU4 enables PPARγ to drive adipocyte browning remains elusive. Here, we report that LKU4 inhibits the expression of PP4C in inguinal white adipose tissue of HFD mice and in insulin-resistant 3T3-L1 adipocytes, which promotes SIRT1-dependent PPARγ deacetylation by activating AMPK, leading to the browning of adipocytes.

The PKA-SREBP1c Pathway Plays a Key Role in the Protective Effects of Lactobacillus johnsonii JNU3402 Against Diet-Induced Fatty Liver in Mice.

Scope: The present study aims to assess the protective effect of Lactobacillus johnsonii JNU3402 (LJ3402) against diet-induced non-alcoholic fatty liver disease (NAFLD) and determine the mechanism underlying its beneficial effect on the liver in mice.

Methods And Results: Seven-week-old male mice are fed a high-fat diet (HFD) with or without oral supplementation of LJ3402 for 14 weeks. In mice fed an HFD, LJ3402 administration alleviates liver steatosis, diet-induced obesity, and insulin resistance with a decreased hepatic expression of sterol-regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC), and an increased phosphorylation of SREBP-1c.

Non-Viable JNU3402 Protects against Diet-Induced Obesity.

In this study, the role of non-viable JNU3402 (NV-LJ3402) in diet-induced obesity was investigated in mice fed a high-fat diet (HFD). To determine whether NV-LJ3402 exhibits a protective effect against diet-induced obesity, 7-week-old male C57BL/6J mice were fed a normal diet, an HFD, or an HFD with NV-LJ3402 for 14 weeks. NV-LJ3402 administration was associated with a significant reduction in body weight gain and in liver, epididymal, and inguinal white adipose tissue (WAT) and brown adipose tissue weight in HFD-fed mice.

Sequential treatment of hydrogen peroxide, vacuum packaging, and dry heat for inactivating Salmonella Typhimurium on alfalfa seeds without detrimental effect on seeds viability.

The aim of this study was to inactivate Salmonella Typhimurium loaded onto alfalfa seeds with sequential treatment of hydrogen peroxide, drying, vacuum packaging, and dry heat. Also, we verified the effect of vacuum packaging in dry heat treatment. Populations of Salmonella on alfalfa seeds after sequential treatment were not detected after 8 or 3 h of dry heat treatment at 70 or 73 °C.

Effect of sequential dry heat and hydrogen peroxide treatment on inactivation of Salmonella Typhimurium on alfalfa seeds and seeds germination.

The purpose of this study was to inactivate Salmonella Typhimurium on alfalfa seeds without having negative effect on seed germination. Inoculated alfalfa seeds were treated with dry heat at 60, 70 or 80 °C for 0, 12, 18 or 24 h followed by 2% hydrogen peroxide solution (10 min). Populations of Salmonella on alfalfa seeds treated with dry heat alone (60, 70 or 80 °C) for up to 24 h were reduced by 0.

Diabetic conditions downregulate the expression of CD2AP in podocytes via PI3-K/Akt signalling.

Background: Proteinuria is typically accompanied by structural and compositional changes of the foot processes and of the slit diaphragms between podocytes. CD2-associated protein (CD2AP) in podocytes serves as an adaptor protein binding to nephrin and podocin, anchoring these slit diaphragm proteins to actin filaments of podocyte cytoskeleton and sending signals inward or outward.

Methods: In the present study, we prepared streptozotocin-induced diabetic renal tissues and cultured podocytes in diabetic conditions to investigate podocyte phenotypical changes, including quantitative and distributional changes of CD2AP protein and search for the signalling mechanisms in diabetic conditions.

Regulation of type IV collagen alpha chains of glomerular epithelial cells in diabetic conditions.

An early feature of diabetic nephropathy is the alteration of the glomerular basement membrane (GBM), which may result in microalbuminuria, subsequent macroproteinuria, and eventual chronic renal failure. Although type IV collagen is the main component of thickened GBM in diabetic nephropathy, cellular metabolism of each alpha chains of type IV collagen has not been well studied. To investigate the regulation of alpha(IV) chains in diabetic conditions, we examined whether glucose and advanced glycosylation endproduct (AGE) regulate the metabolism of each alpha(IV) chains in the diabetic tissue and glomerular epithelial cells (GEpC).

Delay of renal progression in methylmalonic acidemia using angiotensin II inhibition: a case report.

Methylmalonic acidemia (MMA) is a heterogeneous inborn error of propionate metabolism. Management frequently includes a low-protein diet to minimize precursors of methylmalonic acid and reduce its concentration in body tissues. In the long-term follow-up, renal dysfunction in these patients has been increasingly recognized.