It was time to take care of my health. Learn more about its symptoms, causes, and treatment. I learned that the best type 2 diabetes diet is the one that works for you.
Members of the T2D Healthline community understand well how managing diabetes can feel overwhelming. These 6 tips can help make it easier. It's normal to feel overwhelmed or nervous about managing your type 1 diabetes.
While each day will be different, this basic guide can help you stay…. Diabetes can impact almost all the body's systems. Find out more about some diabetes impacts you may not have known about. Health Conditions Discover Plan Connect. Type 2 Diabetes. Medically reviewed by Debra Sullivan, Ph. Types of diabetes Pancreatitis Pancreatic cancer Outlook Diabetes and your pancreas A direct connection exists between the pancreas and diabetes.
Hyperglycemia and hypoglycemia can quickly become life-threatening. Types of diabetes. The diabetes-pancreatitis connection. The diabetes-pancreatic cancer connection. Read this next. What Is Brittle Diabetes? Several cross-sectional studies suggest that visceral fat increases throughout the lifespan in men and women of all ages and race, independent of increases in body weight [ 85 — 88 ]. Gabriely et al. Moreover, removal of VF in Zucker Diabetic Fatty ZDF rats prevented the progressive decrease in insulin action and delayed the onset of diabetes, but VF extraction did not alter plasma free fatty acid levels [ 91 ].
Borst et al. These studies provide verification that VF is a potent modulator of both hepatic and peripheral insulin action [ 92 ]. Calorie restriction CR extends life span and retards age-related chronic diseases in a variety of species, including rats, mice, fish, flies, worms, and yeast [ 93 ].
Our studies have shown that a reduction in fat mass, specifically VF, may be one of the possible underlying mechanisms of the antiaging effect of caloric restriction [ 94 ]. Nowadays, adipose tissue is recognized as an active metabolic-endocrine organ, and obesity is considered as a low-grade inflammatory condition strongly linked to adverse metabolic outcomes. A putative key link between increasing fat mass and obesity-related complications, including insulin resistance, is a chronic low-grade inflammatory state within adipose tissue, related to infiltration by macrophages [ 95 ].
We and others have shown that VF depots display a unique profile of inflammatory mediators compared to subcutaneous adipose tissue, including the clearly higher expression levels of macrophage migration inhibitory factor MIF and chemokine receptor 2 in VF [ 96 , 97 ].
Other studies also suggested that VF is a stronger risk factor for metabolic disorders and mortality than subcutaneous fat [ 82 , 98 ]. MIF knockout mice live longer than the control mice [ ].
Macrophages are considered to be a significant source for many fat-derived proinflammatory cytokines, and the percentage of macrophages in fat has been shown to increase in obesity [ ]. Interestingly, our study suggested that the percentage of macrophages in the stromal vascular cell fraction from both visceral and subcutaneous fat increased with age regardless of obesity status [ ].
Taken together, increase of VF is a hallmark of aging and a source of increased chronic inflammation. Inflammation could accelerate the aging process [ ] and eventually lead to the metabolic dysfunction. Breaking this vicious cycle by decreasing the VF will be a potential therapeutic method for treating metabolic and related diseases Figure 3.
Link between Aging, visceral fat, inflammation, and metabolic syndrome. Visceral fat increases with age and the increase of visceral fat induces inflammation. Inflammation accelerates the process of aging. Lack of or resistance to insulin leads to two metabolic crises: a marked increase in the rate of lipolysis in adipose tissue and activation of hepatic gluconeogenesis in spite of high plasma glucose levels.
The increased rate of lipolysis increases circulating FFA levels, which, in turn, exacerbates insulin resistance in the whole body. It has been very well documented that the acute elevation of plasma FFA produces insulin resistance in both diabetic and nondiabetic individuals [ — ].
It is also shown that chronically elevated plasma FFA levels cause insulin resistance, and lowering elevated plasma FFA levels overnight normalizes insulin sensitivity in obese nondiabetic subjects and significantly improves insulin sensitivity in obese diabetic patients [ ]. The mechanisms by which elevated levels of FFA produce insulin resistance have not been fully understood.
However, studies have shown that increasing plasma FFAs acutely decreases insulin-stimulated glucose uptake and glycogen synthesis in human [ ].
It is also reported that increase of FFA level in human inhibits PI3 kinase activity in skeletal muscle [ ], suggesting the impairment of insulin signaling by FFA. Itani et al. The steatotic liver is also resistant to insulin in terms of inhibition of hepatic glucose production and stimulation of glycogen synthesis.
The high FFA levels may be the unifying mechanism that accounts for the insulin resistance in obesity, type 2 diabetes, lipodystrophy, and aging [ ]. We and others have shown that the circulating FFA levels are significant higher in 9- to month-old SD rats compared to 3-month old, demonstrating that circulating FFA increases with age [ ].
Although peripheral insulin resistance is a hallmark of the development of T2D, more recent evidence has shown that insulin resistance also exists in central nervous system CNS , and that central insulin action plays an important role in regulating whole body glucose metabolism.
Like peripheral tissues, molecules in insulin signaling such as insulin receptor IR , insulin receptor substrates IRS , and phosphatidylinositol 3-kinase PI3K are universally expressed in the brain, indicating a potential role of insulin signaling in the brain.
Koch et al. Gelling et al. Interestingly, an increasing body of evidence shows a link between diabetes and AD, a neurodegenerative disorder and the most common form of dementia.
It has been reported that patients with T2D increase the prevalence of AD by two-to-three folds [ ], and insulin levels and insulin activity in the central nervous system are reduced in AD [ ].
Studies in human subjects show that both peripheral and central administration of insulin improves memory in AD patients [ — ], suggesting impairment of insulin signaling in the brain as a risk factor of neurodegenerative disorders, and restoration of insulin signaling could be a potential therapy for AD. This brings an interesting question whether aging is also associated with central insulin resistance. Fernandes et al. Other studies showed that intracerebroventricular administration of insulin was more efficient at reducing food intake and body weight in 3-month-old rats than in 8- and month-old rats, indicating the development of hypothalamic insulin resistance with age in Wistar rats.
Furthermore, the tyrosine phosphorylation of IR and IRS-2 and the phosphorylation of downstream target genes such as Foxo1 and p70S6K declined, whereas serine phosphorylation of IR and IRS-2 increased with age in rat hypothalamus [ ].
Aging-associated increase in central and peripheral insulin resistance could contribute to both diabetes and AD. The field of central insulin resistance and its role in the development of neurodegenerative disorders and the control of whole body glucose homeostasis is complicated and further studies are needed to fully understand the underlying mechanisms.
For a detailed review of the insulin signaling in the brain, we refer the readers to the following reviews [ 9 , — ]. It is clearly established that the risk for impaired glucose tolerance and diabetes increase with age in rodents and humans. However, the integrated whole body glucose homeostasis is complex with various age-related parameters playing a crucial role on both aspects of glucose homeostasis, namely, insulin action and insulin secretion.
Leptin, a hormone secreted from adipose tissue, plays a key role in energy intake and expenditure. Deficiency of leptin and its receptor leads to severe obesity, insulin resistance, and diabetes in rodents and humans. Resistant to the effects of leptin, termed leptin resistance, is seen in obesity and aging. It has been reported that aging is related to increase in proapoptotic markers with ER stress in multiple tissues, including lung, liver, kidney, and brain [ , ].
In the past decade, a family of nicotinamide adenine dinucleotide- NAD- dependent protein deacetylases, termed sirtuins, have been shown to contribute to longevity. Sirtuins slow aging in worms, fruit flies, and mice [ ]. Interestingly, overexpression of sirtuins or treat with activators of sirtuins, such as resveratrol protect against metabolic decline in aging, increases insulin sensitivity, increases insulin secretion, improves life quality, and extends lifespan [ 11 , , ].
In addition to the above-mentioned variables, aging-associated sedentary life style and diminished physical activity may be important factors for age-related changes of glucose homeostasis. Research has shown that healthy elderly with greater degrees of physical fitness have better glucose tolerance and lower level of insulin resistance than less active old people [ ].
In addition, aging is associated with defects in the balance of insulin secretion and insulin action demands. Our data shows that compared to younger animals, when challenged with a prolonged hyperglycemic stimuli older animals are unable to maintain the insulin secretion proportional to the degree of resistance [ ]. Whole body glucose homeostasis is a complex balance of glucose production and utilization by different tissues. Food intake and hepatic glucose production are the two sources of glucose production, while skeletal muscle contributes to the majority of the glucose uptake and utilization.
Utilizing tracer technology, it is possible to differentiate between the effects on glucose production liver and glucose utilization primarily the muscle. Hepatic glucose production HGP plays crucial roles in glucose homeostasis, both in the fasting and postprandial states. In contrast to rodents, where there is an increase in HGP in age, there are no differences in either the basal hepatic glucose production or the dose-response curve of its suppression by insulin between young and old individuals [ ].
The European Group for the Study of Insulin Resistance reported that hepatic glucose production does not increase with age, when adjusted for lean body mass [ ]. Furthermore, hepatic glucose output has not been shown to be increased in elderly patients with T2D [ ]. Thus, hepatic insulin resistance does not seem play a significant role in decreased glucose tolerance of elderly people [ ].
As mentioned earlier, skeletal muscle is the major source of glucose utilization. Glucose is transported into the cells by glucose transporters.
Through anaerobic and aerobic pathways, glucose is broken down to generate energy. GLUT4 is the major glucose transporter in skeletal muscle responsible for insulin-stimulated glucose uptake. Muscle GLUT4 protein level is not altered in obesity and T2D, however, its expression levels decline with age, and are related to insulin sensitivity in normal controls [ ].
European Group for the Study of Insulin Resistance demonstrated that glucose uptake is not altered as a function of aging per se but is secondary to increased body fat accumulation [ ]. Moreover, the decrease of lean body mass [ ] and contractile strength with age are other factors that contribute to the reduction in insulin stimulated glucose uptake. The above factors, along with changes in body composition, accumulation of VF, and increase in circulating FFA levels, contributes to the decreased glucose uptake with age.
Glucose intolerance, insulin resistance, and T2D associated with aging are leading causes of morbidity and mortality through its multiple complications as well as increases in the risk for multiple other age-related diseases such as cancer, stroke, cardiovascular diseases, Parkinson's disease, and AD [ 6 ].
A comprehensive understanding of all the defects that impair glucose homeostasis in the elderly will lead to development of appropriate, novel treatments that will substantially improve quality of life and over all life span.
The authors thank the members of Muzumdar laboratory for the helpful discussion and critical reading of the manuscript. National Center for Biotechnology Information , U. Journal List Int J Endocrinol v.
Int J Endocrinol. Published online May Zhenwei Gong 1 and Radhika H. Radhika H. Author information Article notes Copyright and License information Disclaimer. Muzumdar: ude. Gong and R. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been corrected. See Int J Endocrinol. This article has been cited by other articles in PMC. Find out how to create a diabetes meal plan and what foods to eat and avoid. Also, learn about healthful meal options for children, including ideas….
A person can manage their diabetes by making healthful changes to their diet, exercising frequently, and regularly taking the necessary medications…. How is the pancreas involved in diabetes? Medically reviewed by Maria Prelipcean, M. The pancreas How is the pancreas linked with diabetes?
Diabetes and pancreatitis Diabetes and pancreatic cancer Other disorders Summary The pancreas is the organ that produces insulin, and it plays a major role in regulating blood glucose levels. What to know about the pancreas. Share on Pinterest The pancreas produces insulin and sits in the abdomen.
How is the pancreas linked with diabetes? Diabetes and pancreatitis. Share on Pinterest Symptoms of pancreatitis can include nausea and fever. Diabetes and pancreatic cancer. Other disorders of the pancreas. Diabetes Endocrinology. Exposure to air pollutants may amplify risk for depression in healthy individuals. Costs associated with obesity may account for 3. Related Coverage. All you need to know about insulin sensitivity factor.
Medically reviewed by Alana Biggers, M. Can you live without a pancreas? Medically reviewed by Graham Rogers, M. People with type 3c diabetes may have mild impairments with blood sugar control, or may have more extreme swings in blood sugar, called brittle diabetes.
This latter condition may be due to having impairments in the hormone glucagon or problems with nutrient digestion and absorption, due to pain or nausea from pancreatitis, or alcohol dependence. Digestive enzyme impairment. Type 3c diabetes impacts the digestive function of the pancreas, causing a condition called exocrine pancreatic insufficiency EPI in nearly every person with chronic pancreatitis and diabetes. Digestive symptoms due to EPI are less common in other types of diabetes, but do still occur in almost one third of type 2 diabetes patients and one to two thirds of type 1 diabetes patients.
How does pancreatitis cause type 3c diabetes? Over time in chronic pancreatitis the pancreas loses the ability to produce enough insulin, and thus to control blood sugar. The ability to release enzymes to help digest food also declines in parallel.
In later stages of the pancreatitis, the scarring of the pancreas destroys the insulin-producing parts of the pancreas. Other causes of diabetes in people with pancreatitis. Rarely, new diabetes in people aged over 50 years turns out to be due to pancreatic cancer. This risk is highest in the first years after diagnosis of diabetes. Nevertheless, the vast majority of people who are diagnosed with new-onset diabetes at those ages solely have diabetes. It should also be noted that individuals with pancreatitis are still able to get type 1 or type 2 diabetes, independently of their pancreatitis.
0コメント