Category: Metabolic Disorders

Categories : Expert Opinion Metabolic DisordersTags :

No More Sugarcoating It: GLP-1s Are a Powerful Weapon in the War Against Sugar

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Photo by Patrick Fore on Unsplash

A new movement in weight management is taking hold in South Africa as the country confronts weight-related illnesses. A powerful class of medication known as GLP-1 therapies is proving highly effective in cutting obesity rates, lowering cancer risk, and improving overall metabolic health. Their growing popularity marks a new frontline in the fight against sugar-driven disease.

A landmark study published in JAMA Oncology has revealed that patients using GLP-1 medications – a class of therapies originally developed for type 2 diabetes – experienced a 17% lower overall risk of cancer.

The data, drawn from over 86 000 patients, showed striking reductions in specific cancers: ovarian cancer risk nearly halved, meningioma cases fell by 31%, and endometrial cancer dropped by 25%.

Dr Tommie Smook, medical practitioner at Dr Smook & Partners (managed by RXME Group), says these findings reinforce the urgent need to fight back against sugar-related disease:

“We are witnessing the medical consequences of unchecked sugar consumption every day in practice. Obesity has become one of the greatest epidemics of our time. If we are serious about safeguarding public health, we must declare a national war on sugar – and GLP-1s are among the most powerful tools we now have to help people reclaim their health.”

What GLP-1s actually do

The body naturally produces GLP-1 – a hormone that regulates blood sugar, appetite, and digestion. GLP-1 medications mimic this process:

            •           They slow stomach emptying,

            •           Reduce hunger and cravings,

            •           Help patients feel satisfied with smaller portions, and

            •           Stabilise blood sugar levels.

The result is sustained weight loss. Clinical trials consistently show patients losing 10-15% of body weight, particularly when therapy is combined with nutrition, exercise, and professional support. In South Africa, several GLP-1s are now formally registered for obesity and chronic weight management.

But the benefits don’t end at weight loss. International studies have demonstrated improvements in cardiovascular health – lowering blood pressure, reducing inflammation, and decreasing the risk of heart attacks and strokes. Emerging evidence also suggests neuroprotective effects, with potential to reduce risks of dementia and Alzheimer’s disease.

From diabetes treatment to disease prevention

“GLP-1s are no longer just diabetes drugs,” says Dr Smook. “They are transforming the way we think about weight, chronic disease, and prevention. When used responsibly under medical guidance, these therapies can change not only waistlines, but lifespans.”

At Dr Smook & Partners, patients gain access to GLP-1 therapy under the supervision of qualified medical doctors. Medications are prepared only through SAHPRA-approved compounding pharmacies, ensuring quality and safety. This is supported by a multidisciplinary team – dietitians, biokineticists, nurses, and sports physicians, providing holistic care.

Here are the five essentials you should consider before starting GLP-1 therapy:

  1. See a doctor first – these medications require proper screening and monitoring.
  2. Think beyond injections – lifestyle, diet, and exercise remain vital.
  3. Expect an adjustment phase – side effects like nausea are usually temporary.
  4. Protect lean muscle – resistance training and adequate protein intake are essential.
  5. Avoid shortcuts – unregulated, black-market products are unsafe and unpredictable.

A turning point for public health

Obesity is a modern epidemic, and sugar is at the heart of it. GLP-1 medications are not a “quick fix,” but they represent one of the most promising advances in decades – a way to tackle both the causes and consequences of excess weight.

Dr Smook concludes: “The stigma around GLP-1s must end. These therapies are not about vanity – they are about survival. Every patient who regains control of their health is one step closer to breaking sugar’s grip on our society.”

Categories : Metabolic Disorders Surgeries & ProceduresTags :

Study Shows Greater Long-Term Benefits of Bariatric Surgery Compared to GLP-1 RAs

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Sleeve gastrectomy. Credit: Scientific Animations CC4.0

A large Cleveland Clinic study has found that people with obesity and type 2 diabetes who undergo weight-loss surgery live longer and face fewer serious health problems compared with those treated with GLP-1 receptor agonist medicines alone.

Patients who had weight-loss surgery (also known as bariatric or metabolic surgery) lost more weight, achieved better blood sugar control, and relied less on diabetes and heart medications over 10 years. The research is published in Nature Medicine.

“Even with today’s best medicines, metabolic surgery offers unique and lasting benefits for people with obesity and diabetes,” said Ali Aminian, MD, director of Cleveland Clinic’s Bariatric & Metabolic Institute and primary investigator of the study. “The benefits we observed went beyond weight loss. Surgery was linked to fewer heart problems, less kidney disease, and even lower rates of diabetes-related eye damage.”

GLP-1 (glucagon-like peptide-1) receptor agonists are a class of medications widely used to treat type 2 diabetes and obesity and to reduce health risks. Both metabolic surgery and GLP-1 medicines improve cardiovascular health and metabolism.

The M6 study (Macrovascular and Microvascular Morbidity and Mortality after Metabolic Surgery versus Medicines) followed 3932 adults with diabetes and obesity who received care at Cleveland Clinic for up to 10 years. Among them, 1657 underwent metabolic surgery (including gastric bypass or sleeve gastrectomy), while 2275 were treated with GLP-1 medicines (including liraglutide, dulaglutide, exenatide, semaglutide, and tirzepatide).

At the end of the study, patients who had metabolic surgery had a:

  • 32% lower risk of death
  • 35% lower risk of major heart problems (such as heart attack, heart failure, or stroke)
  • 47% lower risk of serious kidney disease
  • 54% lower risk of diabetes-related eye damage (retinopathy)

On average, people who had metabolic surgery lost 21.6% of their body weight over 10 years, compared with 6.8% weight loss in people who took GLP-1 medicines. Hemoglobin A1c, a marker of average blood sugar, improved more with surgery (-0.86%) than with GLP-1 medicines (-0.23%). Patients in the surgery group also required fewer prescriptions for diabetes, blood pressure, and cholesterol.

“Even in the era of these powerful new drugs to treat obesity and diabetes, metabolic surgery may provide additional benefits, including a survival advantage,” said Steven Nissen, MD, Chief Academic Officer of the Heart, Vascular & Thoracic Institute at Cleveland Clinic and senior author of the study.

“Our findings indicate that surgery should remain an important treatment option for obesity and diabetes,” said Dr Aminian. “These long-term benefits are harder to achieve with GLP-1 medicines alone, as many patients stop using the medications over time.”

According to the authors, the study has some limitations. It was observational rather than a randomized comparison of drugs and surgery, and it did not focus exclusively on the newest and most effective GLP-1 medicines. The researchers note that future studies should directly compare surgery with newer GLP-1 therapies, such as semaglutide and tirzepatide, to further guide treatment decisions.

Source: Cleveland Clinic

Categories : Metabolic Disorders Substance UseTags :

GLP-1 Receptor Agonists Protect the Liver During Alcohol Consumption

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Photo by Apolo Photographer on Unsplash

GLP-1 receptor agonists are also promising for the treatment of alcohol use disorder and alcohol-associated liver disease, as growing evidence suggests they reduce the motivation to drink alcohol. Now, surprising new findings reveal that the medications may have direct protective effects on the liver as well.

In a new study, published in npj Metabolism Health and Disease, Yale School of Medicine (YSM) researchers found that in mice, GLP-1RAs reduced an enzyme that metabolises alcohol. That, in turn, decreased the production of toxic alcohol metabolites.

“This is the first time that GLP-1 receptor agonists have been shown to regulate alcohol metabolism in the liver,” says principal investigator Wajahat Mehal, MD, professor of medicine (digestive diseases) at YSM. “If you’re taking semaglutide, then your body will likely handle alcohol differently.”

However, because these drugs slowed the metabolism of alcohol, the mice also had higher blood alcohol levels, the researchers found.

“GLP-1 receptor agonists seem to have very similar effects in mice and humans,” says Mehal. “If these results are also reproduced in humans, people using GLP-1 receptor agonists might be drinking an amount of alcohol that does not normally put them above the legal blood alcohol level, but because they are taking this drug, it does.”

Further studies in humans are needed to understand these impacts of GLP-1 receptor agonists more fully, he stresses.

GLP-1 receptor agonists decrease toxic alcohol metabolites

In the study, researchers gave mice either a GLP-1 receptor agonist or a placebo. They observed that mice receiving the medication had decreased levels of a liver enzyme known as Cyp2e1, which breaks down alcohol into a toxic metabolite called acetaldehyde.

“This is significant because alcohol itself is actually not the most toxic molecule to the liver,” explains Mehal. Rather, acetaldehyde is one of the major drivers of alcohol-related harm to the liver. “These drugs are resulting in less acetaldehyde.”

The findings suggest that not only might GLP-1 receptor agonists help the liver by acting on the brain to reduce alcohol consumption, but also through slowing metabolism of alcohol in the liver, and in turn reducing the levels of toxic metabolites.

Ongoing clinical trials are currently testing the benefits of semaglutide for people living with alcohol-induced liver disease. The study suggests that GLP-1 receptor agonists may offer greater benefits to the liver than previously thought, and that the drug may still help patients who are not abstaining from alcohol.

“Even if some individuals don’t reduce their alcohol intake while they’re on a GLP-1 receptor agonist, they will probably still have hepatic protection, because fewer toxic metabolites will be produced in the liver,” Mehal says.

GLP-1 receptor agonists increase blood alcohol concentration

In another experiment, the researchers measured blood alcohol concentrations of mice 30 minutes after giving them alcohol. They found that mice who had received a GLP-1 receptor agonist had higher blood alcohol concentrations compared to controls, and that these levels took longer to drop.

More research is needed to better understand the consequences of elevated blood alcohol levels on the rest of the body, Mehal says.

“If the liver is not metabolizing alcohol as quickly, the alcohol load could be shifted to other organs,” he poses. “Then, not only might people have a high blood alcohol level, but may also experience more cognitive effects like discoordination.”

The number of people taking these drugs is rapidly increasing—as many as one in eight adults in the U.S. have used or are currently using a GLP-1 receptor agonist. Meanwhile, about half of U.S. adults drink alcohol and 6% report drinking heavily.

As the use of these medications for a range of conditions continues to rise, it is increasingly important to study the interactions between these medications and alcohol, Mehal says.

“There already are large numbers of people who are taking GLP-1 receptor agonists and are drinking either social amounts or excess amounts of alcohol,” says Mehal. “We need to know the effects of these drugs in that setting.

Source: Yale School of Medicine

Categories : Metabolic DisordersTags :

Considering Sex Hormones Led to Better Identification of Genes Linked to Type 2 Diabetes

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Genomic and hormone study of white Europeans finds 22 additional disease-related variants

Ball and stick 3D model of testosterone. Source: Wikimedia CC0

Researchers identified almost two dozen previously unknown genetic variants linked to type 2 diabetes by including participants’ hormone levels in their analysis. Yan V. Sun of Emory University, USA, and colleagues reports these findings in the open-access journal PLOS Genetics.

Type 2 diabetes affects an increasing number of people worldwide, and more often affects men than women. The disease is caused by a mix of genetic and lifestyle factors, but little is known about how someone’s environment – both inside and outside the body – interacts with their genes to impact a person’s risk of developing the disease.

In the new study, researchers performed genome-wide interaction studies to investigate whether a person’s hormone levels interact with their genetic variants to affect their risk of developing type 2 diabetes. They grouped males and females independently and considered measurements of three types of sex hormones – total testosterone, bioavailable testosterone and sex-hormone binding globulin. The information came from white European participants in the UK Biobank, which contains biological samples and health data from half a million people.

The researchers used statistical analyses to identify relevant variants in the genomes of individuals with and without type 2 diabetes. By taking into account hormone levels, the analysis was able to identify 22 spots on the genome that increased a person’s risk for type 2 diabetes. These variants had not been reported previously in the most recent genomic study for type 2 diabetes.

The new study suggests that a person’s hormone levels may be interacting with their genes to increase their odds of having type 2 diabetes. For future studies, the researchers recommended that additional hormone measurements for each participant and more diverse cohorts should be included. They conclude that this approach, which includes environmental factors in genomic studies, may help us to identify additional disease-related genes and gain a better understanding of the mechanisms behind complex diseases.

The authors add, “We found that sex hormone levels contribute to differences in genetic risk factors for type 2 diabetes in men and women. By analyzing data for men and women separately, we identified new genetic associations with type 2 diabetes.”

The lead analyst, Amonae Dabbs-Brown notes, “I actually used to work at the CDC developing methods to measure some of these sex hormones. It’s really exciting to see what happens downstream. Maybe one day I’ll even get to see how these analyses are used in the clinic!”

Provided by PLOS

In your coverage, please use this URL to provide access to the freely available paper in PLOS Genetics: https://plos.io/3ViXDKH

Contact: Rob Spahr [rob.spahr@emory.edu]

Citation: Dabbs-Brown A, Liu C, Hui Q, Wilson PW, Zhou JJ, Gwinn M, et al. (2025) Identification of gene-sex hormone interactions associated with type 2 diabetes among men and women. PLoS Genet 21(9): e1011470. https://doi.org/10.1371/journal.pgen.1011470

Author countries: United States

Funding: This work is supported in part by funding from the National Institutes of Health (HL154996 to YVS, DK139632 to YVS, and HL156991 to YVS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. YVS received salary support from the National Institutes of Health.

Competing interests: The authors have declared that no competing interests exist.

Categories : Metabolic DisordersTags :

Unmasking a New Diabetes Subtype in Sub-Saharan Africa

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Photo by Wes Dissy on Unsplash

In this month’s podcast, QuickNews looks at a new Lancet study, “Non-autoimmune, insulin-deficient diabetes in children and young adults in Africa.” In this study, researchers report that a significant subset of what has previously been classified as Type 1 diabetes in sub-Saharan Africa may in fact be a distinct, novel form of the disease.

The individuals in this subset did not exhibit the typical autoimmune markers (islet autoantibodies) usually found in classic Type 1 diabetes in other parts of the world. The researchers instead identified a novel, non-autoimmune, insulin-deficient subtype of diabetes that is also distinct from Type 2 diabetes.

Further evidence of this new subtype was found in Black individuals in the USA, albeit less frequently, but not in White individuals. The discovery throws a spotlight on the heterogeneity of diabetes diagnoses in sub-Saharan Africa, and points to the need to consider alternative causes and explore new prevention and treatment strategies for this distinct form of the disease.

Categories : Metabolic DisordersTags :

Metformin Found to Change Blood Metal Levels in Humans

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Although metformin is the most widely prescribed diabetes drug in the world, its mechanism of action is still not clear. Kobe University endocrinologist OGAWA Wataru has now made significant progress, finding that it changes blood metal levels in humans. Photo by Towfiqu Barbhuiya on Unsplash

The widely used diabetes drug metformin may achieve its effects by changing blood metal levels in humans. The Kobe University study is an important step in understanding the drug’s many actions and designing better ones in the future.

Metformin is the most widely prescribed diabetes drug in the world. Apart from lowering blood sugar levels, it is also known to have a broad range of beneficial side effects such as against tumours, inflammations and atherosclerosis. However, although it has been used for more than 60 years now, its mechanism of action is still not clear, hampering the development of even better drugs against these conditions.

Kobe University endocrinologist OGAWA Wataru says: “It is known that diabetes patients experience changes in the blood levels of metals such as copper, iron and zinc. In addition, chemical studies found that metformin has the ability to bind certain metals, such as copper, and recent studies showed that it is this binding ability that might be responsible for some of the drug’s beneficial effects. So, we wanted to know whether metformin actually affects blood metal levels in humans, which had not been clarified.” To do so, Ogawa and his team enlisted about 200 diabetes patients at Kobe University Hospital, half of which took metformin and half of which did not, in a study to analyse their blood serum levels for those metals and various metal deficiency indicators.

In the journal BMJ Open Diabetes Research & Care, the Kobe University team now published the first clinical evidence of altered blood metal levels in patients taking metformin. They showed that drug-taking patients have significantly lower copper and iron levels and heightened zinc levels. Ogawa says: “It is significant that we could show this in humans. Furthermore, since decreases in copper and iron concentrations and an increase in zinc concentration are all considered to be associated with improved glucose tolerance and prevention of complications, these changes may indeed be related to metformin’s action.”

Recently, Japan has approved the use of imeglimin, a new diabetes drug that is a derivative of metformin but that should not be able to bind metals the same way as its parent. “Imeglimin is thought to have a different method of action, and we are already conducting studies to compare the effects the two drugs have,” says Ogawa.

It is not just about understanding the current drugs, however. Ogawa explains the bigger picture, saying: “We need both clinical trials and animal experiments to pinpoint the causal relationship between the drug’s action and its effects. If such studies progress further, they may lead to the development of new drugs for diabetes and its complications by properly adjusting the metal concentrations in the body.”

Source: Kobe University

Categories : Implants and Prostheses Metabolic DisordersTags :

Implant Treats Type 1 Diabetes by Oxygenating Insulin-producing Cells

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A 3D map of the islet density routes throughout the healthy human pancreas. Source: Wikimedia CC0

Cornell researchers have developed an implant system that can treat Type 1 diabetes by supplying extra oxygen to densely packed insulin-secreting cells, without the need for immunosuppression. The system could also potentially provide long-term treatment for a range of chronic diseases.

The findings appear in Nature Communications. The co-first authors were former postdoctoral researcher Tung Pham and doctoral candidate Lora (Phuong) Tran.

The technology builds off previous implantable encapsulation devices developed in the lab of Minglin Ma, professor of biological and environmental engineering in the College of Agriculture and Life Sciences (CALS) and the paper’s senior author.

Ma has explored a variety of ways to address Type 1 diabetes, which is typically managed through daily insulin injections or insulin pumps, but even with that treatment, patients still suffer the devastating effects of the disease.

Ma’s previous implantable devices have proved effective in controlling blood sugar in diabetic mice, but they can only last so long.

“One of the major challenges is the implant itself often dies due to the lack of oxygen after implantation,” Tran said. “In our lab, they had success in mice that lived over one year, and they controlled the diabetes very effectively with some small capsules without oxygen generation. However, when we scale up, we need more cells, we need more density, especially. We need a higher dose. If we implant without generating oxygen, the cells often die within two weeks.”

Ma’s team developed the new system in collaboration with electrochemical researchers from Giner Inc, including co-author Linda Tempelman, PhD ’93.

The key components of the system are a cylindrical capsule with a ring-shaped cross-section that contains transplanted insulin-secreting cells, and an electrochemical oxygen generator that is roughly the size of a dime and removeable. A nanofibrous membrane outside the capsule protects the cells from the host body’s immune system; a permeable membrane in the core of the capsule allows the central supply of oxygen to reach the ring of cells.

“We have to meet two requirements,” Tran said. “The first is immune protection. And second, you have to maintain mass transfer, like the glucose and other nutrients and molecules that can go in and out.”

Working with Dr James Flanders, associate professor emeritus in the College of Veterinary Medicine, the researchers successfully tested the system in rat models.

“It’s the proof of concept. We really proved that oxygenation is important, and oxygenation will support high cell-density capsules,” Tempelman said. “The capsules are immune protective and last for a long time without having some kind of fouling of the membrane. The body never likes when you put a foreign substance in. So that’s the engineering in the Ma Lab, to look for materials and coatings for the materials that are immune protective, but also don’t invoke excess response from the body because of the material.”

The new system would enable a much greater number of the 2 million people who suffer from Type 1 diabetes in the US to now have an islet transplant or cell therapy without requiring immune suppression, which is considered too dangerous for routine use. Also, the new system can provide much tighter sugar control, effectively curing the disease and enabling the person to eat, drink and exercise like everyone else. 

The next step will be to implant the system in a pig model, and also test it with human stem cells. The researchers are interested in eventually trying to use the system for implanting different cell types in humans for long-term treatment of chronic diseases, according to Tempelman, who is CEO of Persista Bio Inc., a new startup she founded with Ma and Flanders that is licensing these technologies.

“We see an age where people will be getting implants with allogeneic cells from other human beings, from stem cell lines, and using it long term to treat things that your body is missing,” Tempelman said. “Here we’re missing insulin. In pain control, maybe you need more endorphins or some other molecule. In enzyme replacement therapy, you need more enzymes. We’re interested in things like other autoimmune diseases where there’s inflammation that’s out of control.

“So maybe you could put a small molecule in that would treat inflammation, and then someone, like a Lupus patient, wouldn’t have to take an oral medication. They could just have a low-level implant that provides a low amount of it.”

Source: Cornell University

Categories : Metabolic Disorders NeurologyTags :

New Research Shows that Macrophages Help Prevent the Development of Neuropathy

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Source: Pixabay CC0

An increase in high-fat, high-fructose foods in people’s diets has contributed to a dramatic increase in type 2 diabetes. This, in turn, has led to an increase in peripheral neuropathy. About half of people with type 2 diabetes are affected, and of these, about half experience severe neuropathic pain.

The damage begins as axons from sensory neurons begin to retract and disappear from the tissues they innervate. New research from the lab of Clifford Woolf, MB, BCh, PhD, director of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, reveals that months before the damage occurs, immune cells flood into peripheral nerves in an apparent attempt to protect them. This surprising insight, published in Nature, could lead to strategies to prevent peripheral neuropathy or at least minimize and slow the onset of the damage.

Immune cells prevent nerve damage

A team led by Sara Hakim, PhD, a graduate student in the lab, created a mouse model of diabetes induced by a high-fat, high-fructose diet. The model showed that these mice developed all the major features of diabetes within eight to 12 weeks of starting the diet. At about six months, axons in the skin began to degenerate, indicating the presence of neuropathy.

“Diabetic neuropathy takes years, or even decades to develop in humans,” says Hakim, who is now at Vertex. “By using a mouse model in which symptoms slowly develop over months, we were able to catch the progression of the disease over time, and observe those early protective responses when the body is still trying to fight the disease.”

The researchers suspected that peripheral neuropathy is caused by the immune system, so used single-cell sequencing to detect changes in immune cells near sensory neuron axons in peripheral nerves.

One type of immune cell residing in nerves, a pro-inflammatory macrophage, began producing chemokines. These signaling molecules recruited a second population of circulating macrophages, which began infiltrating the nerve 12 weeks after the mice began the diet – as sensory symptoms were starting to appear but before nerve degeneration was seen.

Previously, macrophages were thought to have a pathogenic role in diabetes and were mainly reacting to axon loss. But Hakim, Woolf, and colleagues observed just the opposite.

“To our great surprise, when we blocked infiltration of macrophages into the nerve, neuropathy started getting worse, not better,” says Woolf. “The macrophages were protective. They slowed down the onset of neuropathy and reduced its impact.”

Potential strategies for peripheral neuropathy

The Woolf Lab is now exploring how the infiltrating macrophages protect against peripheral neuropathy. The next step would be to find a way to induce and sustain this protection and identify biomarkers that would flag those people with diabetes who are at risk.

One potential protective strategy might involve accelerating the recruitment of macrophages into nerves; another might involve mimicking their protective function by harnessing compounds they secrete, such as galectin 3.

“Since we could profile the cells and identify what genes they are expressing, we found a number of signalling molecules known to be protective,” says Woolf. “We can now go through that list and check to see which are most active.”

The latest work reinforces the idea that pain isn’t just a disease of neurons, but results from interactions between the nervous system and the immune system. In a study last year, the Woolf Lab discovered thousands of molecular interactions between pain-sensing neurons and different types of immune cells.

Now, the plot is thickening with this example of immune cells acting to prevent painful nerve damage. “We’ve now revealed a novel, slower protective effect of the immune system,” Woolf says.

Source: Boston Children’s Hospital

Categories : Metabolic Disorders NeurologyTags :

The Neurons Responsible for Day-to-day Blood Glucose Regulation

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Photo by Anna Shvets

The brain controls the release of glucose in a wide range of stressful circumstances, including fasting and low blood sugar levels.

However, less attention has been paid to its role in day-to-day situations.

In a study published in Molecular Metabolism, University of Michigan researchers have shown that a specific population of neurons in the hypothalamus help the brain maintain blood glucose levels under routine circumstances.

Over the past five decades, researchers have shown that dysfunction of the nervous system can lead to fluctuations in blood glucose levels, especially in patients with diabetes.

Some of these neurons are in the ventromedial nucleus of the hypothalamus, a region of the brain that controls hunger, fear, temperature regulation and sexual activity.

“Most studies have shown that this region is involved in raising blood sugar during emergencies,” said Alison Affinati, MD, PhD, assistant professor of internal medicine and member of Caswell Diabetes Institute.

“We wanted to understand whether it is also important in controlling blood sugar during day-to-day activities because that’s when diabetes develops.”

The group focused on VMHCckbr neurons, which contain a protein called the cholecystokinin b receptor.

They used mouse models in which these neurons were inactivated.

By monitoring the blood glucose levels, the researchers found that VMHCckbr neurons play an important role in maintaining glucose during normal activities, including the early part of the fasting period between the last meal of the day and waking up in the morning.

“In the first four hours after you go to bed, these neurons ensure that you have enough glucose so that you don’t become hypoglycaemic overnight,” Affinati said.

To do so, the neurons direct the body to burn fat through a process called lipolysis.

The fats are broken down to produce glycerol, which is used to make sugar.

When the group activated the VMHCckbr neurons in mice, the animals had increased glycerol levels in their bodies.

These findings could explain what happens in patients with prediabetes, since they show an increase in lipolysis during the night.

The researchers believe that in these patients, the VMHCckbr neurons could be overactive, contributing to higher blood sugar.

These nerve cells, however, only controlled lipolysis, which raises the possibility that other cells might be controlling glucose levels through different mechanisms.

“Our studies show that the control of glucose is not an on-or-off switch as previously thought,” Affinati said.

“Different populations of neurons work together, and everything gets turned on in an emergency. However, under routine conditions, it allows for subtle changes.”

The team is working to understand how all the neurons in the ventromedial nucleus co-ordinate their functions to regulate sugar levels during different conditions, including fasting, feeding and stress.

They are also interested in understanding how the brain and nervous system together affect the body’s control of sugar, especially in the liver and pancreas.

Source: University of Michigan

Categories : Metabolic DisordersTags :

Kids of Obese Parents More Likely to Develop Obesity due to Inheriting Related Genes

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Mom’s genes play a larger role than dad’s in determining whether kids will be obese

A new study finds that kids with obesity are more likely to have obese parents because they inherit obesity-related genes, and to a smaller extent, are impacted indirectly by genes carried by the mother – even when those genes aren’t passed down. A new study led by Liam Wright of the University College London, UK, and colleagues, reports these findings August 5th in the open-access journal PLOS Genetics.

Studies commonly show that children with obesity often have parents with obesity, but the cause of this trend has been poorly understood. Children may inherit genes from their parents that increase their risk of obesity, or they could be shaped by conditions in the womb, or by the food and lifestyle choices their parents make.

In the new study, researchers investigated the effects of the parents’ genetics on the weight and diet of their children. They looked at a measure of obesity called the body mass index (BMI), along with the diet and genetic data from more than 2500 mother-father-child trios. They focused on obesity related genes in the parents – both the ones that were directly passed down to their children, and the genes that weren’t, but that may indirectly impact weight by shaping the child’s environment, which are called genetic nurture effects. They found that, though mothers’ and fathers’ BMIs were consistently correlated with the child’s BMI, this trend could be mostly explained through the genes that children directly inherit. Genetic nurture effects from obesity-related genes in the mother that were not inherited had a smaller impact, only during the child’s adolescence.

The results suggest that a mother’s BMI may be particularly important for determining a child’s BMI, both due to the effects of genes that children directly inherit, and through indirect nurture effects from genes that weren’t passed down. Meanwhile, fathers had little impact on their child’s BMI, apart from the genes that were directly inherited. The study’s authors suggest that analyses that don’t consider the inherited genes are likely to give misleading estimates of the parents’ influence on a child’s weight.

The authors add, “Our results suggest mother’s weight could affect their children’s weight; policies to reduce obesity could have intergenerational benefits.”

Provided by PLOS