Research Advances

In a study of 1556 pregnant women who gave birth (half of whom had kidney disease), those with kidney disease had a 52% increased likelihood of preterm delivery and a 33% increased likelihood of delivery via cesarean section. Infants born to women with kidney disease had a 71% increased risk of admission to the neonatal intensive care unit or infant death compared with infants born to mothers without kidney disease. Also, kidney disease was associated with a 2.3-times increased likelihood of low birth weight.

When diabetic rats were fed a strain of lactobacillus (a type of bacteria found in the human gut) that was engineered to secrete glucagen-like peptide-1, the animals showed significant increases in insulin levels and were more glucose tolerant than animals fed the parent bacterial strain. The rats developed insulin-producing cells within the upper intestine in numbers sufficient to replace 25% to 33% of the insulin capacity of nondiabetic healthy rats.

Investigators have reprogrammed human skin cells to create induced pluripotent stem cells, which were then coaxed into forming insulin-producing cells through the presence of pancreatic growth factors. When the differentiated cells were transplanted under the kidney capsules of diabetic immunodeficient mice, the animals’ blood sugar levels decreased to normal or near-normal levels over 150 days. In MRI analyses, a 3D organoid appeared as a white patch on the transplanted kidneys but not on control kidneys.

Researchers have uncovered a common gene signature that may help support tolerance following kidney transplantation. A meta-analysis of studies identified a robust gene signature involving proliferation of B and CD4 T cells, and inhibition of CD14 monocytes among 96 tolerant samples. This signature was further supported through a cross-validation approach, yielding 92.5% accuracy.

New research reveals that the effects of salt consumption on the kidneys are mediated at least in part by brain-kidney interactions.

By studying DNA methylation patterns within individuals’ cells, scientists have identified a type of biological clock that provides clues about how long a person is likely to live. In 4 independent studies of almost 5000 older people, each person's biological age was measured from a blood sample at the outset, and participants were followed for up to 14 years. When the DNA methylation age was 5 years higher than the chronological age, individuals had a 16% increased risk of dying during follow-up, after adjusting for various factors.

Recent clinical studies have identified sympathetic denervation as a predictor of increased arrhythmia susceptibility. Now, a new Nature Communications study in mice shows that this risk may be decreased after a heart attack by intervening with intracellular sigma peptide (ISP) to promote axon regeneration into cardiac scar tissue.

Researchers have discovered an insulin-decreasing hormone that exists in both fruit flies and humans. When food is withheld from flies, the hormone limostatin is produced at high levels by nutrient-sensing cells in the gut. Circulating insulin levels increase when flies are genetically engineered to lack limostatin or when a receptor for limostatin on insulin-producing beta cells is blocked.

Researchers have identified a link between changes in gut microbiota and the onset of type 1 diabetes. Researchers followed 33 infants who were genetically predisposed to the condition from birth to age 3. Gut microbiome composition was determined via regular stool sample analysis. Among those children who did develop type 1 diabetes, the team saw a 25% drop in microbial community diversity within the gut. These findings, published in Cell Host & Microbe, might pave the way for microbial-based diagnostic and therapeutic options for patients with type 1 diabetes.

Through studies conducted in mice, scientists have found that IL-6, which is rapidly produced at high levels during glomerulonephritis, potently dampens activation of tissue-destructive macrophage immune cells. Protection relies only on the IL-6 receptors that are bound on macrophage cell membranes. The JASN findings may have broad clinical implications because IL-6-directed therapies are increasingly being used or studied to treat various inflammatory and autoimmune conditions.

Researchers have found that insulin suppresses glucose production by the liver by inhibiting the breakdown of fat, which results in a reduction in hepatic acetyl CoA (a key molecule that regulates the conversion of amino acids and lactate to glucose). They also found that reversal of this process due to inflammation in fat tissue leads to increased hepatic glucose production and hyperglycemia in high-fat-fed rodents and obese, insulin-resistant adolescent animals.

Researchers have created a long-lasting “smart” insulin that self-activates when blood sugar soars. Tests in a mouse model of type 1 diabetes show that one injection of Ins-PBA-F works for a minimum of 14 hours, during which time it can repeatedly lower blood sugar levels after mice are fed sugar. As described in a PNAS paper, Ins-PBA-F consists of a long-acting insulin derivative with a phenylboronic acid (PBA) moiety on one end.