A look at the latest research

United States Most Expensive Place to Have T2D

People with type 2 diabetes in the U.S. have the highest healthcare costs to treat the disease in the world, according to a recent study published in PharmacoEconomics. The lifetime price tag to treat T2D in the U.S. is around $283,000, even higher than in other countries with comparable income levels.

Researchers led by Till Seuring, of the University of East Anglia’s Norwich Medical School in the United Kingdom, provided a systematic review of the global evidence on the cost of T2D. They identified data from 109 studies — 86 cost-of-illness (COI) and 23 labor market — in the largest global review of the economic impact of diabetes.

The team found that direct costs were generally higher than indirect costs. They wrote, “Direct costs ranged from $242 for a study on out-of-pocket expenditures in Mexico to $11,917 for a study on the cost of diabetes in the USA, while indirect costs ranged from $45 for Pakistan to $16,914 for the Bahamas.” Seuring and his team went on to write that direct diabetes costs appear to be closely and positively associated with a country’s gross domestic product (GDP), “and that the USA stood out as having particularly high costs, even after controlling for GDP per capita.”

Diabetes hits poor countries the hardest since they have to bear higher costs burdens, and that’s compounded by the fact that two-thirds of all cases of diabetes are now in low- and middle-income countries such as China, India, Mexico, and Egypt.

Seuring said in a statement: “Our findings underline the fact that diabetes not only has strong adverse effects on people’s health but also presents a large — and at least partly avoidable — economic burden. We also found that the economic burden of diabetes increases over time. So early investments into prevention and disease management may therefore be particularly worthwhile. For both rich and poor countries, the results mean that better prevention and management of diabetes has the potential to not only bring good health but also economic gains. We would hope that the findings further increase the policy attention being paid to diabetes prevention and management in rich countries and it should in particular make health and economic policymakers in developing countries aware of the economic damage that diabetes can do.”

KISSPEPTIN Expressed in Mouse Leydig Cells

Kisspeptin is expressed in mouse Leydig cells, meaning it may play an important role in male reproduction, according to a study recently published in Endocrinology.

Researchers led by Sajad Salehi, MD, of Johns Hopkins School of Medicine, noted that kisspeptin has been reported to be expressed in peripheral tissues, including the testes, but “factors regulating testicular kisspeptin and its role in reproduction are unknown.” So Salehi and his team set out to address kisspeptin’s function in the testis and to determine the level of kisspeptin in the testis in comparison with the brain and other tissues, “how these levels change from the prepubertal period through sexual maturation, and the factors involved in kisspeptin regulation in the testis.”

The investigators used immunohistochemical analysis of testis sections in mice with a validated kisspeptin antibody localized kisspeptin to the Leydig cells. They did not find kisspeptin in germ cells or Sertoli cells within the seminiferous tubules at any developmental time period studied, from prepuberty to sexual maturation. However, they did find that kisspeptin was expressed in the mice’s Leydig cells, and that in vitro and in vivo studies indicated clearly that luteinizing hormone (LH) is involved in regulating levels of Leydig cell kisspeptin. “Interestingly,” the authors wrote, “gonadectomy resulted in elevated LH but reduced serum kisspeptin levels, suggesting that testicular kisspeptin may be secreted. These data document kisspeptin expression in mouse Leydig cells, its secretion into peripheral serum, and its regulation by changes in reproductive neuroendocrine function.”

The researchers pointed out that these data raise questions about where within the testes kisspeptin is present, when during testicular development it appears, how it is regulated, and what it does. They concluded that “kisspeptin is present in Leydig cells, developmentally responsive, and regulated by neuroendocrine mechanisms controlling LH. We propose that Leydig cell kisspeptin may play a pivotal role in peripheral and neuroendocrine modulation of male reproduction.”


Korean researchers have found that “night owls” are more likely to develop diabetes, metabolic syndrome, and sarcopenia than early risers, even when they get the same amount of sleep, according to a new study published in The Journal of Clinical Endocrinology & Metabolism.

The study, led by Nan Hee Kim, MD, PhD, of Korea University College of Medicine in Ansan, Korea, examined sleeping habits and metabolism in 1,620 participants in the population-based cohort Korean Genome Epidemiology Study (KoGES). The study subjects were between the ages of 47 and 59. Participants responded to questionnaires about their sleep-wake cycle, sleep quality, and lifestyle habits. Researchers took blood samples to assess participants’ metabolic health, and the study subjects underwent DEXA scans to measure total body fat and lean mass, and CT scans to measure abdominal visceral fat. Based on the questionnaire results, 480 participants were classified as morning chronotypes, and 95 were categorized as evening chronotypes. The remaining participants had a sleep-wake cycle between the two extremes.

Even though the evening chronotypes tended to be younger, they had higher levels of body fat and triglycerides than morning chronotypes. Night owls also were more likely to have sarcopenia. Men who were evening chronotypes were more likely have diabetes or sarcopenia than early risers. Among women, night owls tended to have more belly fat and a great risk of metabolic syndrome.

“Regardless of lifestyle, people who stayed up late faced a higher risk of developing health problems like diabetes or reduced muscle mass than those who were early risers,” Kim says. “This could be caused by night owls’ tendency to have poorer sleep quality and to engage in unhealthy behaviors like smoking, late-night eating, and a sedentary lifestyle.”

DOPAMINE Shows Anti-incretin, Anti-proliferative Action on ß-Cells

Dopamine (DA) may regulate insulin secretion from β-cells and play an important role in homeostasis of β-cell mass, which could explain bariatric surgery’s effects on type 2 diabetes, according to a study recently published in Molecular Endocrinology.

Researchers led by Antonella Maff ei, PhD, of Columbia University, noted that human islet β-cells exploit an autocrine DA-mediated inhibitory circuit to regulate endocrine secretion. Th ey also pointed out that in humans, a mixed meal stimulus is accompanied by contemporary serum excursions of incretins, DA, and its biosynthetic precursor L-3,4-dihydroxyphenylalanine (L-DOPA). That suggests that DA may act as an anti-incretin as postulated by the foregut hypothesis proposed to explain the early effects of bariatric surgery on type 2 diabetes.

So the investigators took a “translational step backwards” to characterize the kinetics of plasma DA and incretin production after a mixed meal challenge in a rat model and study the integration of incretin and DA signaling at the biochemical level in a rodent β-cell line and islets. “We found that there are similar excursions of incretins and DA in rats, as those reported in humans,” the authors wrote, “after a mixed meal challenge and that DA counters incretin enhanced glucose-stimulated insulin secretion and intracellular signaling at multiple points from dampening calcium fluxes to inhibiting proliferation as well as apoptosis.”

The researchers concluded based on their results that DA is an important regulator of insulin secretion and may represent one axis of a gut level circuit of glucose and β-cell mass homeostasis.

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