In 1996, Dr. Wayne Lautt and his colleagues first discovered a hormone they originally called hepatic insulin-sensitizing substance (HISS). In 2021, they renamed this hormone “hepatalin” (hepata from the medical word for liver and lin from insulin).
Through their ongoing research, Dr. Lautt and his Scimar team have determined that it is important for hepatalin and the hormone insulin to be in healthy balance.
Hepatalin, when adequately produced, stimulates the body’s ability to partition glucose into muscle. When the liver does not adequately produce hepatalin, the pancreas produces additional insulin, which causes nutrient energy to be partitioned into fat.
Their work is keenly focused on this process of “Nutrient Partitioning” and on developing a series of “NuPa” products to measure metabolic health and to stimulate the production of hepatalin.
Science has proven that this essential secretion of hepatalin is hindered by stress, lack of exercise, consumption of sugar, and other lifestyle factors.
Therefore, the goal of Scimar’s work is to determine ways for the body to always produce the right amount of hepatalin and to keep hepatalin and insulin in a healthy balance.
The science tells us that when the right amount of hepatalin is present, nutrient partitioning is in balance, thereby helping people to avoid type 2 diabetes. For those already living with type 2 diabetes, managing hepatalin effectively is expected to help people avoid the disease’s worst impacts.
Changing the focus to hepatalin and nutrient partitioning will change the prevention and treatment paradigms in diabetes.
Eating food results in glucose absorption for immediate use as energy, while the excess is stored in our muscle cells as “glycogen” or in fat cells as “triglycerides.” This distribution of glucose is called nutrient partitioning and it helps determine our wellbeing.
If nutrient partitioning is optimal, our muscles store most of the glucose. If it is poor, more glucose gets stored as fat.
Dr. Lautt’s extensive research demonstrated clearly that hepatalin is mainly responsible for glucose storage in muscle. If the liver cannot produce enough hepatalin, our pancreas compensates by producing more insulin, causing nutrient energy to partition into fat.
Eating food activates two permissive signals, increased hepatic glutathione (GSH) and a parasympathetic signal to the liver acting via acetylcholine (ACh), on muscarinic receptors to activate nitric oxide (NO) release. Both signals are needed to trigger hepatalin release.
Blocking any pathway will block hepatalin from being released, causing hepatalin-dependent insulin resistance. Post-meal blockage of hepatalin release accounts for postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, and increased oxidative stress.
Chronic hepatalin-dependent insulin resistance results in progressive and predictable dysfunctions typical of obesity and type 2 diabetes.
Dr. Lautt, Professor Emeritus at the Department of Pharmacology and Therapeutics at the University of Manitoba, has about 220 peer-reviewed publications to his credit. Of these, over 60 are related to HISS (renamed “hepatalin” in 2021), including the following:
- Hepatic parasympathetic (HISS) control of insulin sensitivity determined by feeding and fasting
- Meal-induced Insulin Sensitization in Conscious and Anesthetized Rat Models Comparing Liquid Mixed Meal with Glucose and Sucrose
- Synergistic Protection by S-adenosylmethionine with Vitamins C and E on Liver Injury Induced by Thioacetamide in Rats
- HISS-dependent Insulin Resistance (HDIR) in Aged Rats is Associated with Adiposity, Progresses to Syndrome X, and is Attenuated by a Unique Antioxidant Cocktail
- Meal-induced Insulin Sensitization (MIS) and its Parasympathetic Regulation in Humans
- Bethanechol and N-acetylcysteine Mimic Feeding Signals and Reverse Insulin Resistance in Fasted and Sucrose-induced Diabetic Rats
- Absence of meal-induced insulin sensitization (AMIS) in aging rats is associated with cardiac dysfunction that is protected by antioxidants
- Lifestyle Impact on Meal-induced Insulin Sensitization in Health and Prediabetes: a Focus on diet, antioxidants, and Exercise Interventions
- Obesity as an Early Symptom of the AMIS Syndrome